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A TEXT-BOO I 



DENTAL PATHOLOGY 



AND 



THERAPEUTICS 



FOR STUDENTS AND PRACTITIONERS 



BASED UPON THE ORIGINAL OF 



HENRY H. BURCHARD, M.D., D.D.S. 

LATE SPECIAL LECTURER ON DENTAL PATHOLOGY AND THERAPEUTICS IN T THE PHILADELPHIA 

DENTAL COLLEGE 



REWRITTEN BY 

OTTO E. IXGLIS, D.D.S. 

PROFESSOR OF DENTAL PATHOLOGY AND THERAPEUTICS IN THE PHILADELPHIA 
DENTAL COLLEGE 

SIXTH EDITION, THOROUGHLY REVISED 
ILLUSTRATED WITH 735 ENGRAVINGS AND A COLORED PLATE 




LEA & FEBIGER 

PHILADELPHIA AND NEW YORK 

1920 



*% 



Copyright 

LEA & FEBIGER 

1920 



JUN 10 1320 



CI.A571247 



THIS 

VOLUME 

IS RESPECTFULLY DEDICATED 

TO 

RUSSELL H. CONWELL, D.D., LL.D. 

IN RECOGNITION OF HIS UNSELFISH 

EFFORTS IN THE 

OPENING OF OPPORTUNITIES 

FOR EDUCATION. 



PREFACE TO SIXTH EDITION. 



In revising this work for a new edition, the editor has endeav- 
ored to maintain the original idea of a text-book, furnishing a 
description of each dental disease and its treatment in such manner 
that teachers may find it a useful adjunct in the presentation of 
the subject of dental pathology and therapeutics to their students. 
Since the last edition a reprint has been necessary, owing to an unex- 
pectedly large demand by the Government, and in consequence of 
this and the almost revolutionary changes which have occurred 
in the professional thought and because of natural developments 
from scientific investigations many changes have had to be made. 
It has been thought advisable to omit certain chapters dealing 
with subjects which are better covered in other approved text- 
books and to include new chapters upon subjects which are 
germane to dental pathology. Thus, chapters on Prophylaxis, 
Radiography, Plantations, The Uses of Electricity in Therapeutics 
and Root Amputation have been inserted. Many new illustra- 
tions have been added to take the place of some omitted and to 
enhance the elucidation of the subjects. 

Wherever quotations appear an endeavor has been made to credit 
the author, the idea to be presented has been the compelling 
motive rather than the writing of a history. Quotations have 
generally been made from current literature and from as limited 
a bibliography as possible in order that this work may have value 
added to it by reference to books and journals within easy reach 
of any who desire further details. The editor desires to thank 
those who have kindly loaned illustrations, and the publishers for 
their generous treatment, also the profession for its continued 
favor. O. E. Inglis. 

1524 Chestnut Street, Philadelphia. 



CONTENTS. 

SECTION I. 
GENERAL PATHOLOGY. 

CHAPTER I. 

General Principles 17 

CHAPTER II. 
Disturbances of the Vascular System . 21 

SECTION II. 
ABERRATIONS IN ERUPTION OF THE TEETH. 

CHAPTER III. 
Dentition: Its Progress, Variations, and Attendant Disorders . 63 

CHAPTER IV. 
Malformation and Impaction of Teeth 115 

SECTION III. 
DEVELOPMENTAL ABNORMALITIES. 

CHAPTER V. 

Malformations and Anomalies of the Teeth 133 

SECTION IV. 

ACQUIRED NON-SEPTIC AFFECTIONS OF THE ENAMEL 

AND DENTIN. 

CHAPTER VI. 
Abrasion, Erosion, and Mechanical Injury 199 

CHAPTER VII. 

Stains of the Enamel and Dentin 232 



viii CONTENTS 

SECTION V. 
DENTAL CARIES AND HYPERSENSITIVE DENTIN. 

CHAPTER VIII 

Dental Caries: History; Exciting and Predisposing Causes . . 241 

CHAPTER IX. 
Dental Caries: Pathology, Morbid Anatomy, and Clinical History 273 

CHAPTER X. 

Dental Caries: Diagnosis, Symptoms, and Prognosis 301 

CHAPTER XL 

Dental Caries: Therapeutics and Prophylaxis 337 



SECTION VI. 
DISEASES OF THE DENTAL PULP. 

CHAPTER XII. 
Constructive Diseases 359 

CHAPTER XIII. 

Destructive Diseases of the Dental Pulp 380 

CHAPTER XIV. 
Methods of Removal of the Dental Pulp and Root-canal Filling 428 

CHAPTER XV. 
Gangrene of the Pulp 4S1 



SECTION VII. 
DISEASES OF THE PERICEMENTUM. 

CHAPTER XVI. 
Pericementitis 511 



CONTENTS ix 

CHAPTER XVII. 

Chronic Septic Apical Pericementitis 535 

CHAPTER XVIII. 

Non-septic Pericementitis 56S 



SECTION VIII. 

PERICEMENTAL DISEASES BEGINNING AT THE 
GUM MARGIN. 

CHAPTER XIX. 
Gingivitis 603 

CHAPTER XX. 

Salivary and Serum al Calculus 62 S 

CHAPTER XXI. 
Pyorrhea Alveolaris 649 

CHAPTER XXII. 
Pericemental Abscess 69S 

CHAPTER XXIII. 
Reflex Neuroses 705 

CHAPTER XXIV. 

Infections of and from the Mouth, and Sterilization .... 719 

CHAPTER XXV. 
Prophylaxis 747 

CHAPTER XXVI. 

Dental Radiography 701 

CHAPTER XXVII. 
Apicoectomy and Root Amputation 771 

CHAPTER XXVIII. 

Plantation of Teeth 777 

CHAPTER XXIX. 
The Uses of Electricity in Dental Therapeutics 783 

CHAPTER XXX. 

Asepsis and Sterilization 793 



DENTAL PATHOLOGY AND THERAPEUTICS. 



SECTION I. 
GENERAL PATHOLOGY. 



CHAPTER I. 
GENERAL PRINCIPLES. 

General pathology (pathos, disease, and logos, & discourse) is that 
branch of science which treats of the modifications in function and 
changes in structure occurring in disease. It embraces all patho- 
logical processes occurring in the human body, and as many of these 
occur in and about the teeth, modified only by the peculiar anatomy 
of the parts, Dental Pathology may be said to be that branch of 
dental science which treats of modifications in function and changes 
in structure occurring in the diseases of the teeth and associate parts. 

This being true, it follows that the study of dental pathology must 
be preceded by a study of the general disease processes which affect 
the tissues of the body, and such of these as are applicable to the 
study are known as the General Principles. 

The word Therapeutics is derived from the Greek therapeuein, to 
take care of, meaning the measures adopted to remedy or remove 
the changes induced by pathological processes. 

The study of the pathology of a part begins with a study of its 
anatomy and histology, then naturally follows a study of its physi- 
ology and embryology. These form the basis from which degrees 
of abnormal function and altered structure may be judged by com- 
parison with similar processes occurring in other parts of the body. 

This altered function and structure theoretically go hand in hand, 
as whichever begins first the other surely follows even if only to a 
microscopic degree. Disease, in its broad sense, is therefore an altera- 
tion of nutrition, resulting in changes in function and structure. 
The term Disease refers to the various classified pathological con- 
2 (17) 



18 GENERAL PRINCIPLES 

ditions. each occurring in a more or less definite way and having 
sufficiently defined characteristics to render them distinct from each 
other. The sequence of cause, effect upon the circulation and the cells, 
the alterations in the function and structure of the cells and of the 
part or body as a whole, together with the terminations of disease, 
are embraced in the term Pathology. The term Morbid Anatomy 
refers more particularly to the changes in structure. 

A disease cause may be defined as any influence of whatsoever 
nature which is capable of disturbing the nutritive balance of any 
portion of the body. 

The study of disease causes is called Etiology. The signs of 
disease obtainable by vision, hearing, touch, smell, taste, micro- 
scopic examination or chemical analysis are termed the Objective 
Symptoms. Such sensations or effects as are described by the 
patient are the Subjective Symptoms. The study of both kinds is 
Symptomatology. 

The grouping of all the clinical phenomena of a particular disease 
is its Clinical History. 

The distinction of a present disease from all others by means of 
its symptoms is Diagnosis, and its probable outcome judged from the 
existing phenomena and the usual clinical history under such circum- 
stances is Prognosis. 

The cause which directly produces a disease is known as the excit- 
ing cause, while a condition, either local or systemic, which favors its 
action is known as a predisposing cause (see those of Dental Caries). 
A Proximate Exciting Cause is one which exerts its effect directly 
upon the cells, while a cause back of this and to which the proximate 
cause may be due, is a Primary Exciting Cause. 

The proximate exciting causes may be conveniently grouped into: 

1. Abnormal Food Supply, a condition of the blood which contains 
substances improper for the cells, or lacks constituents they need, or 
the cells are supplied with too much or too little lymph (food). 

2. Abnormal Waste Removal, either due to circulatory disturbance 
causing retention of the waste of cells about them when it should be 
removed, or as a fault of some excretory organ (primary cause) 
retaining waste of cells in the blood as a whole. 

3. Abnormal Physical Conditions, such as direct injuries, mechani- 
cal interference with the cells or their circulation, or chemical effects 
including the action of microorganisms. 

4. Abnormal Nerve Supply, such as excessive or defective innerva- 
tion. 

In a general way all living cells, including microorganisms, have 
common life conditions which may be grouped as follows: 



PATHOGENESIS 19 

1. A proper food supply, including water and oxygen, though 
some bacteria seem to do better in the absence of oxygen and plants 
require carbon dioxid. 

2. A proper removal of waste products. 

3. Proper physical conditions, including a proper temperature. 

4. Possibly a proper innervation, though this does not apply to 
microorganisms. 

As disease conditions are alterations of nutrition, due mainly to 
change in life conditions, the above classification of proximate 
exciting causes is justifiable. 

From the standpoint of dental pathology, exciting causes may again 
be divided into (1) septic or those due to bacteria or protozoa and 

(2) aseptic or non-septic, such as the mechanical, chemical and ner- 
vous, the resulting diseases being also broadly classifiable into septic 
and non-septic, each class having many dental representatives. 

In the production of pathological conditions by a disease cause 
the part may (1) be injured directly after which the process of pathol- 
ogy starts in the tissue injured if death of all cells be not immediately 
produced, but if death of cells occurs, the process begins in the adjoin- 
ing living cells or (2) the cells may be stimulated, all their functions 
being increased either within semi-physiological bounds or stimulated 
to the point of weariness and exhaustion. The substance of the cells 
is lost in overwork, and if not promptly replaced, degeneration ensues. 

(3) The cells may be reduced in activity by lessened temperatures, 
retained waste products or lack of food supply, lessened innervation, 
etc., and all of their functions reduced. They gradually pass through 
atrophy, degeneration and death, owing to altered metabolism. (4) 
Cells may be altered in character by infiltration of materials derived 
from other sources into their substance or they may be individually 
injured by microorganisms. 

The origin and progress (Pathogenesis) of a disease being known, 
intelligent efforts may be made for its prevention. This is Prophy- 
laxis. 

The science of prevention of disease upon the broad basis of a 
knowledge of disease causes and observance of laws of health is 
Hygiene. 

It will be seen that a knowledge of special pathology can only be 
obtained from (1) a knowledge of pathology in general or at least of 
those principles of general pathology which underlie all disease pro- 
cesses; (2) a knowledge of the local anatomy and histology; (3) a 
knowledge of local embryology and physiology; (4) a study of local 
pathology and morbid anatomy. To this must be added a study of 
materia medica arid special therapeutics. 



20 GENERAL PRINCIPLES 

"When treatment is based on pathogenesis and a parallel knowledge 
of the action of drugs and remedies, it is termed Rational Thera- 
peutics. When based upon known good effects of a drug or remedy, 
without knowledge of its action, it is termed Empirical Thera- 
peutics. 

In this work merely the most important general principles are 
included, the reader being referred to works on general pathology 
for subjects not touched upon. 





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OHAIHN BY J.N Z CnASt 



BLOOD. 

(Ehrlich triple stain.) 
(Prepared by Dr. I. P. Lyon.) 

Fig. I. TYPES OF LEUCOCYTES. 

a. Polymorphonuclear Neutrophile. b. Polymorphonuclear Eosinophile. c. Myelocyte 
(Neutrophilic), d. Eosinophilic Myelocyte, e. Large Lymphocyte (large Mononuclear). 
/. Small Lymphocyte (small Mononuclear). 

Fig. II. NORMAL BLOOD, 
field contains one neutrophile. Reds are normal. 

Fig. III. AN/EMIA, POST-OPERATIVE (secondary). 

The reds are fewer than normal, and are deficient in haemoglobin and somewhat 
irregular in form. One normoblast is seen in the field, and two neutrophiles and one 
small lymphocyte, showing a marked post-hsemorrhagie anaemia, with leucoeytosis. 

Fig. IV. LEUCOCYTOSIS, INFLAMMATORY. 

The reds are normal. A marked leucoeytosis is shown, with five neutrophiles and 
one small lymphocyte. This illustration may also serve the purpose of showing the 
leucoeytosis of malignant tumor. 

Fig. V. TRICHINOSIS. 
A marked leucoeytosis is shown, consisting of an eosinophilia. 

Fig. VI. LYMPHATIC LEUKAEMIA. 

Slight anaemia. A large relative and absolute increase of the lymphocytes (chiefly 
the small lymphocytes) is shown. 

Fig. VII. SPLENO-MYELOGENOUS LEUKAEMIA. 

The reds show a secondary anaemia. Two normoblasts are shown. The leucoeytosis 
is massive. Twenty leucocytes are shown, consisting of nine neutrophiles, seven myelo- 
cytes, two small lymphocytes, one eosinophile (polymorphonuclear) and one eosinophilic 
myelocyte. Note the polymorphous condition of the leucocytes, i.e., their variations 
from the typical in size and form. 

Fig. VIII. VARIETIES OF RED CORPUSCLES. 

a. Normal Red Corpuscle (normocyte), b, c. Anaemic Red Corpuscles, d-g. Poikiloeytes. 
ft. Mieroeyte. i. Megaloeyte. j-n. Nucleated Red Corpuscles. j,k. Normoblasts. I. Micro- 
blast, to, n. Megaloblasts. 



CHAPTER II. 



DISTURBANCES OF THE VASCULAR SYSTEM. 



A suitable amount and quality of blood normally flows through 
the arteries, capillaries and veins, and is in close relation to processes 
of nutrition occurring in the lymph channels or adjunct circulatory 
apparatus. 

The amount of blood in the vessels may be increased (plethora), 
though not permanently. It may be decreased rapidly in quantity, 
as by hemorrhage, or its red corpuscles may be gradually lessened 
in number (acute or chronic anemia) . The proportion of white cor- 
puscles to red ones may be increased abnormally (leukemia). The 
hemoglobin of red corpuscles may be deficient (chlorosis). Locally 
the amount of blood in a part may be increased (hyperemia or 
inflammation) or diminished (ischemia). 

Normally the blood contains floating in the plasma 5,000,000 red 
corpuscles, or erythrocytes, and from 5000 to 10,000 (1 to 500 red) 
white corpuscles, or leukocytes, to each cubic millimeter. (See Plate, 
Fig. II.) A marked increase in the number of erythrocytes is termed 
polycythemia; a marked decrease, oligocythemia. The temporary 
increase in number of white corpuscles is leukocytosis, a temporary 
fall is leukopenia; a persistent increase, leukocythemia or leukemia. 

The blood corpuscles may be classified as follows: 

See Plate, 
Fig. 1 Fig. VIII 

Normocytes (normal size) . 



Erythrocytes (non-nu- 
cleated red corpuscles) 



Normal to 
blood. 



. . 1,2,3,4. a 

Microcytes (small size) h 

Pathological I Macrocytes (large size) 

indicators. | Megalocytes (very large size) i 

Poikilocytes (irregular form) d e f g 



Erythroblasts (nucleated ( 
red corpuscles derived J Pathological 
indicators. 



from red marrow 
bones) 



of 



{Normoblasts (normal size) 
Microblasts (small size) 
Megaloblasts (large size) . 



3h 

I 
m n 



Leukocytes (white cor- 
puscles) . 



Normal to 
blood. 



Fig 

Lymphocytes (small) 22% 

Lymphocytes (large) 6 " 

Polymorphonuclear neutrophiles . . 70 " 
Polymorphonuclear eosinophiles . . 2 " 



See Plate, 
1 Fig. I 

5 / 

6 e 

7 a 

8 b 



p , . . . j Basophilic leukocytes or mast cells. 

... -j Neutrophilic myelocytes from bone-marrow . 
[ Eosinophilic myelocytes 



(21) 



22 



DISTURBANCES OF THE VASCULAR SYSTEM 
Fig. 




Normal blood (triacid stain): 1, normal red cell, flatly spread and evenly stained; 
2, normal rouleau; 3, normal red cells varying slightly in size, thickly spread, show- 
ing central clear areas; 4, normal red cell, of slightly altered shape; 5, lymphocyte, 
medium size; 6, large mononuclear leukocyte, incurved nucleus; 7, polynu clear 
neutrophile leukocyte; 8, eosinophile leukocyte. Separate nuclear lobes. (Schmaus 
and Ewing.) 



ANEMIA. 

Anemia is a condition in which the blood is lessened in quantity 
or partly deprived of its essential constituents — i. e., red corpuscles 
and hemoglobin — in consequence of which the tissues receive less 
oxygen and the general nutrition is impaired. 

Acute Traumatic Anemia occurs as a result of copious hemor- 
rhage. The individual becomes temporarily pale and weak. The 
arterial pressure is lessened, the circulation slowed, and the pulse 
is frequent and small. Recovery is, as a rule, prompt, the water 
being first restored and later the corpuscles being regenerated. 1 
Frequent hemorrhages cause the blood to become watery and debility 
results from impaired nutrition. (See Plate, Fig. III.) 

1 Ziegler, General Pathology. 



ANEMIA 23 

Symptomatic Anemia. — A diminution in the number of red cor- 
puscles may occur as a result of protracted overwork, anxiety, study, 
or long-continued illness, such as a fever. 

The number of red blood corpuscles may be reduced to one-half the 
normal amount, and there is a corresponding debility. The condition 
may disappear with appropriate removal of the cause. 

Chlorosis. — This is a form of anemia occurring, for the most part, 
in girls and young women, and characterized by a great deficiency 
in the hemoglobin of the red corpuscles without a corresponding 
reduction in the number of the red corpuscles. In the watery blood 
very small red corpuscles (microcytes) are seen; also a few very 
large ones (macrocytes), and some of irregular outline (poikilocytes). 1 
Myelocytes are occasionally seen. (Stengel.) The pathology is 
uncertain. If prolonged, the red corpuscles may sink in numbers 
to 3,000,000 or 2,000,000 per cubic millimeter and 20 per cent, of 
hemoglobin. 

Being, as a rule, readily cured by a course of iron, it is inferred 
that the body is starved of iron, an essential constituent of hemo- 
globin. It is often associated with gastric disturbances, constipation, 
defective hygiene, and irregular habits, and also has been associated 
with oral sepsis, which apparently have a casual relation. The skin 
and mucous membranes are pale and have a slightly greenish tinge. 2 
In recovery the number of corpuscles is first increased, then the 
hemoglobin. 

Leukocytosis. — This is not a form of anemia, but a temporary 
increase in the number of multinucleated leukocytes, apparently 
derived from the lymphoid structures of the body in response to 
some demand for leukocytes. Thus it occurs normally after a full 
meal, in the later months of pregnancy (13,000) or in the postpartum 
state [15,000], pathologically after hemorrhage, in acute fevers, in 
tuberculosis, in sarcomas and in conditions accompanied by suppu- 
ration. 3 Its presence during the course of surgical disease has been 
held to be diagnostic of pus formation 4 — e. g., in abdominal surgery 
from 8000 to 40,000 per cubic millimeter. In general above 10,000 
is regarded as leukocytosis 20,000 to 50,000 as hyperleukocytosis. 
(See Plate, Fig. IV.) In its opposite leukopenia the white cells may 
be about 4000 per cubic millimeter, 6000 being about the dividing 
line. Infectious diseases are usually accompanied by it. 5 

Leukemia. — Leukemia is a disease characterized by a consider- 
able increase in the number of white corpuscles of the blood, by a 

1 Green, Pathology and Morbid Anatomy. 

2 Ibid. s ibid. 

4 Cabot, Boston Medical and Surgical Journal. 5 See works on General Pathology. 



24 DISTURBANCES OF THE VASCULAR SYSTEM 

diminution in the number of the red corpuscles, and by enlargement 
of some of the lymphatic organs. The proportion of one white to ten 
red corpuscles is common (1 to 5 often, occasionally 1 to 1). The 
spleen may be hypertrophied (splenic leukemia). The lymphatic 
glands may be hypertrophied (lymphatic leukemia). In these latter 
cases the blood contains an excess of uninuclear leukocytes. It is rare 
except when combined with other forms. When the marrow of bones 
is hypertrophied (myelogenic leukemia) large mononuclear leukocytes 
with neutrophile granules are found 1 (myelocytes) and the lympho- 
cytes and polymorphonuclear forms are increased. 2 The blood con- 
tains toxic substances generated by the destruction of leukocytes, 
xanthin bodies, and acids (lactic, acetic). The urine frequently 
contains an excess of xanthin bases and lactic acid. (See Plate, 
Figs. VI and VII.) 

Pernicious Anemia. — This is a comparatively rare but generally 
fatal disease, characterized chiefly by a great fall in the number of 
red corpuscles to one million or less per cubic millimeter, those 
remaining being altered in form and size and showing evidences of 
degeneration. The total hemoglobin is reduced, but the relative 
amount may be increased. Degeneration is shown by peculiarities 
of staining. Normal red corpuscles (normocytes), nucleated red 
corpuscles (megaloblasts), large nucleated red corpuscles (giganto- 
blasts), microcytes, and poikilocytes are found. The blood platelets 
and leukocytes are somewhat diminished. 3 The oxygen-carrying 
power is markedly lessened and all tissues suffer from malnutrition. 
The power of coagulation of the blood is lessened. Marked fatty 
degeneration of the heart muscles is apt to occur 4 as well as fatty 
changes in the kidneys and liver. 

The causes are obscure, but gastro-intestinal disorders, intestinal 
parasites, pregnancy and lactation, hemorrhages, malaria, syphilis, 
tuberculosis, and infections are the chief causes supposed to produce it. 

Aplastic anemia is a severe type of progressive pernicious anemia, 
in which the bone-marrow fails to develop myelocytes and erythro- 
blasts owing to lack of marrow cells (hypoplasia of bone-marrow.) 

COAGULATIVE DISTURBANCES AND HEMORRHAGE. 

The blood when drawn from the body or in contact with a wounded 
surface of injured vessel wall undergoes a process of solidification 

1 Ziegler, General Pathology. 

2 Stengel, A Text-book of Pathology. 

3 Green, Pathology and Morbid Anatomy. 
* Ibid. 



COAGULATIVE DISTURBANCES AND HEMORRHAGE 25 



called coagulation. The nature of the process is in some doubt, but 
it is now thought that the following reactions occur: 1 

Thrombogen + Thrombokinase = Thromboplastin 

(in leukocytes and platelets.) (in platelets and tissue.) 

Thromboplastin + Antithrombin = Prothrombin 
Prothrombin + Calcium salts = Thrombin 

Thrombin + Fibrinogen = Fibrin 

(in the plasma.) 

Fibrin entangling corpuscles = Clot. 

Fibrin forms a network, in the open spaces of which the corpuscles 
are entangled (Fig. 2). Occurring after an accident or surgery 
opening bloodvessels, coagulation causes the cessation of hemorrhage 
by plugging the vessels with a thrombus (or clot within the living 
vessel). In the case of a ligated artery this extends to the next 
anastomosing branch. The filling of vacant spaces such as abscess 
cavities or alveoli of teeth after extraction, also assists, not only in 
checking hemorrhage, but also acts as a scaffold for the granulation 
tissue, which brings about regeneration of the part. The clot is grad- 
ually absorbed (see page 56) . In inflammation the lymph exudate 
may coagulate in the tissue spaces, apparently an effort to limit or 
define the area by blocking up the lymphatics. Coagulation may 
occur in the living vessel, as a thrombus, or in the interstitial tissue, 
as in inflammation and infarction. 

Thrombosis. — The formation of thrombi or clots within the 
living vessel may occur in the heart, arteries, veins, or capillaries. If 
the blood stream be somewhat retarded, an increased number of 
white corpuscles and blood platelets occupy the peripheral zone and 
adhere to the vessel wall. If the vessel wall be injured, the blood 
platelets become attached to it. With these platelets the white 
corpuscles and sometimes the red become deposited. Fibrin forms 
and the corpuscles are included. The thrombus is red when red 
corpuscles are included in it; white when only white corpuscles are 
present. The causes of thrombosis are these: (1) a retardation of 
the blood current at some point from some cause; (2) local changes 
in the walls of the vessels and (3) probably pathological changes in 
the blood. 2 

Older thrombi are firmer than those recently formed. Thrombi 
are also formed in the capillaries, a circumstance which favors the 
spontaneous cessation of hemorrhage. 3 They may form in the vessels 
in inflammation. 4 Remaining in the situations in which they were 
formed, they either undergo simple or puriform softening or are 

1 Howell, Text-book of Physiology. 

2 Ziegler, General Pathology. 

3 See above. 4 See page 38. 



26 



DISTURBANCES OF THE VASCULAR SYSTEM 



calcified, or are resorbed and replaced by connective tissue. (See 
Regeneration.) The calcified varieties are called phleboliths in the 

veins; arterioliths in the arte- 
Fig. 2 ries. The effect of a thrombus 

is to obstruct circulation in the 
degree in which it closes the 
lumen of the vessel. Thus in 





o o ft M o, 
o *-o \° ^it- 



Fibrin filaments and blood tablets. 
A, network of fibrin, shown after 
washing away the corpuscles from a 
preparation of blood that has been 
allowed to clot; many of the fila- 
ments radiate from small clumps of 
blood tablets; B (from Osier), blood 
corpuscles and elementary particles 
or blood tablets within a small vein. 



Fig. 4 




A thrombus in the saphenous vein, 
showing the projection of the conical 
end of the thrombus into the femoral 
vessel: S, saphenous vein; T, throm- 
bus; C, conical end projecting into 
femoral vein. At v, v, opposite the 
valves, the thrombus is softened. 
(Virchow.) 




Diagram to show phenomena of 
venous thrombosis: v, v, valves of veins, 
a, b, primary thrombus (white); c, d; 
s, /, g, secondary white thrombi con- 
nected with primary white thrombus 
by various red thrombi; h, piece of white 
thrombus becoming detached by blood 
current. If septic this would be a possible 
cause of septic infarction (or pyemic meta- 
stasis) . (Green, modified from Thoma.) 



(1) trauma it plugs it completely, obstructing hemorrhage; (2) 
occurring in an artery (not by trauma) it tends to cause ischemia of 
a part supplied by it and may cause necrosis (dry gangrene) by lack 



COAGULATIVE DISTURBANCES AND HEMORRHAGE 27 

of food supply (nutrition) ; (3) in a vein it tends to prevent return 
of blood to the heart (venous hyperemia) and if this is partial, de- 
generation is produced, if total, necrosis (moist gangrene) . A clot in 
a vessel may extend a great distance (Figs. 3 and 4). 

Embolism. — Portions of the softened varieties of thrombi may 
become detached and float about in the blood; these are called 
emboli. Other foreign substances may act as emboli — e. g., air or 
fat globules. In important parts it may cause local anemia, paralysis, 
or slow or rapid death (Fig. 5). 



Fig. 5 



Fig. 6 




Embolus impacted at the bifurcation 
of a branch of the pulmonary artery, 
showing the formation of thrombi be- 
hind and in front of it, and the exten- 
sion of these as far as the entrance of the 
next collateral vessels: E, embolus; t, 
V ', secondary thrombi. (Virchow.) 




Diagram of a hemorrhagic infarct: 
a, artery obliterated by an embolus (e) ; 
v, vein filled with a secondary throm- 
bus (th); 1, centre of infarct which is 
becoming disintegrated; 2, area of 
extravasation; 3, area of collateral hy- 
peremia. If caused by an infective 
embolus an abscess may result. (O. 
Weber.) 



If the thrombus be septic, as in the case of puriform softening, the 
emboli may lodge in small vessels and cause secondary septic disease 
processes, as, for example, in the cases of pyemia accompanied by 
infarctions in which multiple metastatic (or miliary) abscesses are 
formed, each causing local injury and acting as a fresh focus of infec- 
tion as well (see page 47 and below). 

Infarction. — When an embolus occludes a terminal artery, that 
is, an artery whose branches spread like those of a tree without 
anastomosis, the part first becomes ischemic, but soon the backward 
pressure from the vein upon the blood in the capillaries causes an 
extravasation of blood into the interstitial tissue of the wedge-shaped 
area, forming what is called a hemorrhagic infarct. A clot forms 



28 DISTURBANCES OF THE VASCULAR SYSTEM 

degeneration of the clot occurs, and if aseptic it is absorbed and 
replaced by connective tissue (see Regeneration); if caused by a 
septic embolus, it may be involved in the resulting septic process — 
e. g., in pyemic metastatic abscess. Infarction has been held by 
Black to occur in the dental pulp, but he has not proved the case as 
he distinctly describes infarction as the stasis of venous hyperemia, 
quite a different condition. 1 A demonstration has been made by 
Hopewell-Smith of a pulp disease which might be infarction, yet hav- 
ing from the description certain characteristics of venous hyperemia. 
(See Infarction of Dental Pulp.) (Fig. 6.) 

Hemorrhage.— By hemorrhage is meant the escape of blood from 
the vessels. It may be arterial, venous, or capillary. If the vessel 
is ruptured, it is hemorrhage by rhexis. If it occurs by diapedesis, 
as in infarction (into the tissue spaces), it is hemorrhage by diapedesis. 
The diapedesis occurs through the capillary wall rather than the 
stomata; pressure is the cause. Hemorrhage usually ceases spon- 
taneously through thrombosis, as previously described. 

If hemorrhage occurs into the tissues it receives the following 
designations, the escape itself being called an effusion or extravasation: 

Ecchy?nosis, an effusion of moderate extent into tissue beneath a 
surface, as into subcutaneous tissue. 

Petechia the same, but small and circumscribed. 

Suffusion the same when an extensive area is involved. The term 
also covers the staining of bone or dentin by hemoglobin, e. g., suffusion 
of dentin of the crown and root in venous hyperemia of the pulp. 

Infarction, when the area involved is that supplied by terminal 
and non-anastomosing arteries as above described. 

Hemorrhage involves an injury to vessels by traumatism, or 
disease rendering them incapable of retaining the blood, or by 
increased internal pressure, as in violent exertion, or in congestion 
of local vessels, as in venous hyperemia, or as the result of diminished 
external atmospheric pressure, as in high altitudes. The extra vasated 
blood may be absorbed or deposited in the tissues, as in a bruise; 
or excite inflammation or cyst formation (extravasation cyst) . Acute 
hemorrhages or repeated extravasations lead to anemia (which see). 
The extravasated corpuscles may be disintegrated and the hemo- 
globin broken up into varying compounds having various colors. This 
is hematogenous pigmentary infiltration and may be seen in a bruise. 
The colors are often permanently deposited. The color changes may 
occur in some degree in teeth suffused through venous hyperemia 
or the hemoglobin may be modified by pulp putrefaction (see Pulp 

» Special Dental Pathology, p. 257 (Ed. 1915). 



COAGULATIVE DISTURBANCES AND HEMORRHAGE 29 

Putrefaction and Bleaching of Teeth) . As seen in a bruise the extra- 
vasations produce the following pigmentary infiltrations: 

(a) Hemoglobin, dark red. 

(b) Hemin, reddish-brown or bluish-black. 

(c) Methemoglobin, brownish-red. 

(d) Hematin, dark-brown or bluish-black. 

(e) Hematoidin, orange or reddish-brown (light pea green (Jakob)). 
(/) Hemosiderin, yellowish or brownish. 

Hemorrhagic Diathesis. — This is a condition, largely hereditary, 
in which coagulation does not close wounds readily, and ordinarily 
trivial wounds may, in spite of surgical aid, induce death by hemor- 
rhage. Hereditary hemorrhagic diatheses (hemophilia) is usually 
transmitted through the female to the male descendants — i. e., from 
grandfather to grandson through the grandfather's daughter — and 
seven or more generations of hemophilics have been recorded. 1 
Males suffer more than females in the ratio of about 11 to 1. 

In a family of 207 members, in four generations, 37 were hemo- 
philics, all of the male sex; almost half died from hemorrhages, 
usually in infancy, while in the living the tendency to bleed lessened 
as they grew older. 2 

According to Legg, 3 "It is of three degrees of severity: 

"1. Characterized by external and internal bleedings of every 
kind, and by joint affections. 

"2. By spontaneous hemorrhages from mucous membranes, but 
no traumatic bleeding or ecchymoses, and no joint affections. 

"3. A tendency simply to ecchymoses. The first seen most 
frequently in men, the second in women; the third may appear 
in either sex." 

The joint affections are due to hemorrhage, and simulate rheumatic 
affections. Hemophilics are apt to be thin-skinned, neurasthenic, 
and liable to sudden flushings and vasomotor disturbances. 1 Blondes 
suffer more than brunettes. 4 

The injured part may bleed from the first, or a normal clot may 
form and secondary hemorrhage or capillary oozing occur. Death 
may rapidly occur, or the patient bleed to fainting or until almost 
dead, and hemorrhage then cease. This may require any period, 
even weeks. One case is said to have continued for a year. 5 

The pathology of the condition is uncertain. Fillebrown 6 reports 
a fatal case in which the arteries were excessively thin. Porter 7 points 

1 Porter, International Dental Journal, 1900. 

2 Losser, International Journal of Surgery. 

3 Musser, Medical Diagnosis. 4 Thompson, Practical Medicine. 

6 Scott, Dental Cosmos, 1912, p. 60. P International Dental Journal, 1900. 

7 Porter, Loc. cit. 



30 DISTURBANCES. OF THE VASCULAR SYSTEM 

out that the blood may clot in the receptacle, yet not in the small 
vessels of the wound, and infers that some hereditary deficiency exists 
which interferes with the action of the vasoconstrictors. 

Hemophilics usually manifest a history of bleeding before puberty, 
and hemophilic infants have died from hemorrhage due to gum- 
lancing, circumcision, etc. Certain surgical cases in which secondary 
hemorrhages have been due to the action of the continuous use of 
acetanilid have been reported. 

Treatment of Hemorrhage.— Hemorrhages in general are controlled 
or prevented upon four local and three systemic principles which may 
be combined for more rapid effect. 

1 . Mechanically obstructing the flow of blood by ligatures, hemo- 
static forceps, compression of the artery leading to the part, pressure 
of tampons upon the open bleeding vessels which may be reinforced 
by compresses and in case of the jaws forcible closure of the teeth 
upon the compress by a Barton or other bandage. Elevation and 
rest of the part counteract gravity and muscular propulsion. In a 
severe hemorrhage upon the palate, as after lancing, finger pressure 
may be used or a vulcanite or even a modelling compound plate, 
made to produce pressure. 1 In alveolar hemorrhage clots about 
which hemorrhagic leakage occurs, should be removed before packing 
the alveolus. 

2. Injury of the white corpuscles. This liberates the ferments 
necessary for coagulation. It has been noted that lacerated wounds 
bleed less than smoothly cut ones. An implantation may be done 
with rough reamers almost bloodlessly as compared with an extrac- 
tion. The mechanical treatment probably acts in some degree upon 
this principle aside from obstructing the flow of blood. The torsion 
of a tooth-pulp before removal causes the same effect. Actual cau- 
terization does the same. Torsion of an artery in a wound acts upon 
the same principle. 

3. Local vasoconstriction is attained by the use of astringents in 
case of small injuries, as upon the gum, or combined with the tampons, 
as in a tooth alveolus. Tannic acid, alum (both powdered), Monsel's 
solution, ethereal pyrozone, adrenalin or suprarenin solution (in case 
of hemophilia, potassium permanganate made into a paste with 
vaseline is recommended) are examples of this principle. It is also 
exemplified by the effect of cold applications and by the blanching 
effect of adrenalin or suprarenin either in the hypodermic injection 
(with cocain or novocain) or superficially applied for prevention of 
hemorrhage, as in nasal surgery, or for reduction of conjunctivitis. 

i Jojy: Dental Cosmos, 1909, p. 488. 



COAGULATIVE DISTURBANCES AND HEMORRHAGE 31 

4. Coagulation of the albumin of the blood. This may be produced 
by drugs applied locally, many of the astringents having this effect, 
as for example, deliquesced chlorid of zinc, strong silver nitrate 
solutions, alum or tannic acid in powder or solution. The actual 
cautery also coagulates by heat as well as injury of the leukocytes. 
Hall suggests having ready absorbent cotton first wet with a saturated 
solution of alum in distilled water and then dried. 1 

The three systemic principles are: 

1. General vasoconstriction to be used in capillary hemorrhage 
(and avoided in those from cut arteries as in these hemorrhage 
would be increased). Probably this increases friction thus causing 
injury of leukocytes. For this purpose there are employed, dilute 
sulphuric acid (20 to 30 minims pro re nata), oil of Erigeron cana- 
densis, 20 minims on sugar pro re nata, ergot (of the wine, a tea- 
spoonful each two hours, of the fluidextract one-half teaspoonful 
each two hours) suprarenal extract (as adrenalin 1 to 1000) intra- 
venously drop by drop up to 10 minims (Stevens) or grains 10 
by mouth in the form of dried extract. Tannic acid or gallic acid, 
10 grs. in pill pro re nata. Aqueous extract of Hamamelis, teaspoon- 
ful pro re nata, or the fluidextract, 20 minims pro re nata. The 
following is a practical prescription having marked vasoconstricting 
action: 

1$ — Acidi gallici gr. xxxvi 

Pulveris digitalis gr. xij 

Ergotini . gr. x 

Pulveris opii gr. vj 

M. et pone in capsulas, No. xij (M. R. Taylor attributes to Hare). 

2. Increasing the coagulability of the blood. This treatment is 
based upon supplying the blood with calcium salts or some constit- 
uent necessary to the coagulation process. In actual hemorrhage 
calcium chlorid in a massive dose of 75 grs. in solution in water by 
mouth (or clyster if necessary), or 20 grs. by mouth followed by 5 grs. 
each hour up to 5 or 6 doses (Hare). Strontium lactate, 15 grs. 
pro re nata, 2 calcium lactate first dose 20 grs., 5 grs. each hour and 
increasing to 20 grs., sodium sulphate grs. iss every two hours. 3 

Lederer has suggested the injestion of as many raw eggs as the 
patient can bear during a period of thirty-six hours before operation. 4 
P. Emile Weil has suggested the injection of 20 c.c. of fresh human, 
horse, or rabbit serum before operation, for the prevention of hemor- 

1 Dental Cosmos, 1916, p. 949. 

2 Scott: New Jersey Dental Journal, October, 1913. 

3 Reverdin: Dental Cosmos, February, 1904, p. 162. 

4 Dental Digest, 1914, p. 262. 



32 DISTURBANCES OF THE VASCULAR SYSTEM 

rhage in hemophilics, or every three months as a curative measure. 1 
Beam and Dolmage 2 successfully checked a persistent, dangerous, 
eleven-day hemorrhage in a hemophilic by injecting intravenously 
120 c.c. of fresh horse serum, followed by 30 c.c. forty-eight hours 
later as a further preventive. Dr. E. W. Scott 3 reports the use of 
30 c.c. of normal serum by large hypodermic syringje as immediately 
curative of a hemorrhage lasting two and a half days after extrac- 
tion, and 20 c.c. as curative in three to four hours in a case of stab 
wound. Both were blacks. The back was selected as the site of 
injection. To obtain human serum he suggests a willing volunteer, 
not a black or relative, a large blister to be raised. H. A. Schell 4 treated 
a case of hemorrhage persistently recurrent after packing of alveolus 
with (1) Brewster's hemostatic, (2) gauze with tannic acid, (3) gauze 
with alum, (4) gauze with plaster of Paris, (5) gauze with adrenalin, 
compress and bandages being also used. After the five failures within 
eight days, Hemoplastin (Parke, Davis & Co.) 2 c.c. was injected sub- 
cutaneously with success. This preparation is stated "to contain 
prothrombin and anti-antithrombin, the antithrombin, which would 
vitiate the action of the prothrombin, having been eliminated" and 
"to have both a local hemostatic action when applied on gauze 
and to increase the coagulability of the blood when subcutaneously 
administered and not to produce dangerous possibilities such as 
thrombosis and anaphylactic shock or toxic effect." The average 
dose is 1 to 2 mils, repeated every four to six hours until control 
of hemorrhage is obtained. It is furnished in sterile bulbs. Being 
proved and a product of a reliable house and readily available it should 
have early trial in all severe hemorrhages. It has been used with 
success as a prophylactic, preventing hemorrhage in bleeders with 
history of hemorrhage at previous operations. 

In known hemophilics, with operation unavoidable, calcium chlorid, 
gr. iij ter in die for not more than four days, may be given and the 
operation performed. After four days the coagulability of the blood 
is decreased (Hare). In the writer's hands this has allowed almost 
a bloodless extraction in a hemophilic. It disturbs the stomach 
somewhat. Doses of ergot for a less period might be used previous 
to operation. The danger of ergot gangrene (from intense vaso- 
constriction) should always be borne in mind. 

3. Mechanical rest of mind and body is necessary in serious cases 
of hemorrhage to avoid muscular propulsion, rupture of ligated 
vessels, or disturbance of bandages. The use of tincture of aconite in 

1 Dental Cosmos, 1908, p. 346. 

2 Dental Items of Interest, March, 1915. 3 Ibi4-, January, ]012. 
4 Private Communication. 



LOCAL DISTURBANCES OF THE CIRCULATION 33 

small repeated doses slows the heart action. Food should be withheld 
from hemophilics and the hunger relieved with small doses of opium 
and thirst by iced water in small quantities or bits of cracked ice. 
Individuals known to be hemophilics should live a hygienic life, 
avoid all injuries however slight, in the hope of an eventual out- 
growing of the condition. The acute anemia induced by prolonged 
hemorrhage requires treatment by hematics, although in healthy 
individuals the blood lost by a moderate hemorrhage is rapidly 
replaced after feeding with nutritious foods. 

LOCAL DISTURBANCES OF THE CIRCULATION. 

The amount of blood in a part may be increased or diminished. 
The types of local disturbance differ as to causes, phenomena and 
effects, and as to the indicated treatment for each. In health the 

Fig. 7 




Ramification of nerves and termination in the muscular coat of a small artery 
of the frog. (Arnold, Kirke's Physiology). 

bloodvessels are maintained at a proper caliber through the action 
of the vasomotor nerves, disturbances of which permit dilatation of 
the arteries, as is generally the case in arterial hyperemia. On the 
other hand, simple mechanical retention of blood may cause dilata- 
tion or, better, expansion of the veins, as in venous hyperemia. 

Ischemia. — This is local anemia due to (1) obstruction of an 
artery leading to a part or pressure upon the part causing emptyness 
of capillaries; (2) substitution of the blood by fluid as in hypodermic 
injections (enhanced if vasoconstringents as suprarenin are con- 
joined). The condition may be but temporary. If continued the 
effects are those due to lack of nutrition, i. e., atrophy, degeneration, 
necrosis. 
3 



34 DISTURBANCES OF THE VASCULAR SYSTEM 

Arterial Hyperemia. — Inhibition of vasoconstrictor nerve fibers or 
stimulation of vasodilators causes a dilatation of arterial vessels. 
The muscular coat loses its tone and relaxes. The blood, there- 
fore, increases in volume. If the irritation does not carry the part 
beyond this state and into inflammation the condition is a simple 
excess of blood in the arteries and arterial capillaries with the motion 
increased and denominated arterial hyperemia. 

Cause. — It is probable that the cause of vasodilatation is a vaso- 
motor impulse excited in response to a sensory impulse sent to the 
brain from the irritated part. The specific irritants are many. 
(See Arterial Hyperemia of Pulp.) 

Results. — Obviously the good arterial blood in excess produces 
excess nutrition with consequent excess of all functions. The part 
is reddened, more capable of functions, the arterial walls overnour- 
ished by blood (via vasavasorum) and may be thickened in continued 
cases; enlargements of parts occur (hypertrophy by cell growth and 
reproduction) in continued cases. The temperature is increased, 
owing to increased chemical change (oxidation, etc.), and the part 
is more sensitive to all external impressions owing to the increased 
function of the nerves (resulting in hyperesthesia). In the hard 
tissues increased depositions occur, the tissue becoming more dense 
(osteosclerosis — tubular calcification in dentin, etc.), or added to, as 
in secondary dentin, hypercementosis of roots, exostosis, etc. See Index. 

The above is true of the milder, continued grades; in more marked 
cases some pain of throbbing character or disturbance of nutrition 
may occur. It is to be remembered that being due to irritation it 
may involve in some cases a degree of mild inflammation and in the 
dental pulp a venous hyperemia of greater or less degree. Its effects 
are, however, often evidence of its long-continued action either as a 
pure condition or as an association with inflammation as one of its 
zones (the outer). (See Pulp Diseases and page 40.) 

Hyperemia as a Resistance to Infection. — According to Biers and 
others the induction of hyperemia in an infected part increases the 
opsonic power of the excess blood, and therefore is antagonistic to 
infection. No doubt this is the natural process in inflammation. It 
has been occasionally noticed that stimulation, as in the use of a 
capsicum plaster in acute apical abscess, has produced resolution. 
Usually confined abscesses are enlarged and not cured by such 
stimulation. 

Venous Hyperemia (Mechanical or Passive). — Venous hyperemia 
is a collection of blood in the veins due to 

1. Prevention of its passage through the vein on the way to the 
heart by some obstruction (pressure on vein, thrombus in vein, etc.). 



LOCAL DISTURBANCES OF THE CIRCULATION 



35 



2. Lack of propulsive force usually in the heart whereby the arte- 
rial column of blood cannot force a proper circulation and the blood 
tends to collect in the more dependent parts. This may involve 
diminished cardiac power, valvular disease, arterial rigidity or 
obstruction or valvular incompetency of veins. 

The second cause has only a remote dental interest. The first is 
involved in venous pulp hyperemia and is the cause of the second 
stage of inflammation. It is also a means of therapeutics invoked 
when it is desired to induce some forms of Bier's hyperemia, as for 
example, in the use of the stasis bandage about the neck in local anes- 
thesia, the object here being to slow the circulation away from a part 
to be injected by retaining the blood in the head. 

Pathology. — The veins are dilated, the current is slowed, and the 
intravenous pressure is increased, in consequence of which watery 
(serous) exudations occur in the 
parts about them (edema). For FlG - 8 

the same reason in marked cases 
diapedesis of red corpuscles may 
occur (hemorrhage by diapedesis) , 
and their hemoglobin may be dis- 
solved out. The blood in the parts 
not being sufficiently changed, 
and in some cases in a state of 
stasis, there is a lessened food 
supply and waste removal, and 
cell nutrition suffers accordingly. 
Vital processes are lessened, secre- 
tion is diminished, there is less oxi- 
dation, and hence less heat is pro- 
duced and less work is done. Fatty 

degeneration or atrophy occurs in partial cases and in more complete 
cases necrosis may occur, as stasis prevents the access of food supply 
(arterial blood). Long-continued venous hyperemia with great intra- 
venous pressure may produce dropsies. If the walls of the veins are 
weak and are permanently distended or thicken under pressure and 
become tortuous, the condition is called varicosity of the veins (vari- 
cose veins). The exudate of venous hyperemia differs markedly 
from that of inflammation (Fig. 8). 1 




Venous hyperemia of the liver. Two 
capillaries near central hepatic vein, 
showing the thickening of the walls and 
the accumulation of red blood corpuscles 
within them. X 500. (Green.) 



Hyperemic Exudate. 
Poor in albumin. 
Rarely coagulates in the tissue. 
Contains few cells. 
Low specific gravity. 
Contains no peptone. 



Park' 



Inflammatory Exudate. 
Rich in albumin. 
Usually coagulates in the tissue. 
Contains numerous cells. 
High specific gravity. 
Contains peptone (product of cell 
disintegration) . 
Surgery. 



36 DISTURBANCES OF THE VASCULAR SYSTEM 

This is probably due to an increased permeability in the vessel wall 
in inflammation permitting the albumin of the blood to pass through 
and to chemical changes. 

INFLAMMATION. 

Inflammation may be defined as a series of hyperemic changes 
expressive of the reaction of living tissue to irritation, and character- 
ized chiefly by an excessive emigration of leukocytes and exudation 
of coagulable lymph from the bloodvessels. 

Etiology. — Any irritant or injury capable of producing a lesion of 
the bloodvessel wall not involving its immediate death can produce 
inflammation. In case direct death is produced, the inflammation, 
if any, occurs in the tissue contiguous to the dead part. 

The causes of inflammation may be divided first into non-septic 
and septic or infective. The non-septic causes may be extrinsic or 
intrinsic. The extrinsic non-septic causes are: (1) Physical irritants, 
such as violence, mechanical irritation, pressure or traumatism, 
excessive heat or cold, and electrolytic action. (2) Chemical irri- 
tants — e. g., the action of acids, caustics, etc. (3) Nervous or vital 
irritants — e. g., rubefacients, epispastics, arsenic, etc. These act 
only on living tissue through the medium of the nerves. 

An intrinsic non-septic cause may produce inflammation — e. g., 
urates in tissue, mechanical strains upon tissue, temporary lack of 
blood in a vessel or central nervous disturbance, as in herpes from 
locomotor ataxia. 

Non-septic causes, as a rule, produce only such mild inflammatory 
phenomena as are concerned in circumvallation of an irritant, 
absorption of it, and in repair or production of new tissue. No 
pus is produced unless pyogenic bacteria gain ingress. This class 
of inflammation is termed simple inflammation. (For further explana- 
tion see Xon-septic Pericementitis.) 

Septic or Infective Causes. — These are fungi or their products, 
and the classes of inflammations produced are much more severe, 
continuous, and destructive in their nature, and are termed infective 
inflammations. 

Pathology of Simple Inflammation. — If to the web of a frog's foot 
tincture of capsicum be applied, or if its mesentery be exposed to the 
air, and either be examined under the microscope while the animal is 
living, it is noted that after a possible short period of contraction of 
the arterioles dilatation of arteries at once begins and is gradually 
followed by dilatation of the veins and capillaries. This continues 
to steadily increase for about twelve hours. During the first hour 



INFLAMMATION 



37 



of this period the blood current is accelerated and the first stage 
of an inflammation is thus an arterial hyperemia. Following this 
acceleration the blood flow is increasingly retarded. The retardation 
is due to the action of the leukocytes, large numbers of the mono- 
nuclear and polymorphonuclear forms of which fall out of the central 
blood stream into the periaxial stream and collect along the walls of 
the small veins (Fig. 9, b). Several layers of leukocytes may thus 
form. Probably some peculiar attraction exists between the leuko- 
cytes and the wall of the vessel, or a positive chemotaxis exists as in 
infective inflammation. 

Fig. 9 




Small vein in mesentery of dog, after exposure for half an hour and irrigation with 
salt solution : a, red corpuscles ; b, leukocytes adhering to wall of vein ; c, red corpuscles; 
d, leukocytes which have escaped from vessel; e, leukocyte in act of escaping; /, 
fibrous tissue. X 340. Modified from Thoma. (Green.) 



This massing of leukocytes compels the red corpuscles to the 
center of the stream (Fig. 9, a), and their passage is mechanically 
interfered with; thus the further dilatation of the vessel becomes 
a process of venous hyperemia. The vessels are increased in size 
and length and become more tortuous. Pulsation is noted. 

Coincident with retardation of the blood flow, the leukocytes are 
seen to work their way by an ameboid movement through the walls 
of the veins and to some extent of the capillaries into the perivascular 
spaces — i. e., into the adjoining tissue — in which they may move far 
from their point of escape and mass about the irritant if one be 
present. This process is called emigration (Fig. 9, e). At the same 



38 DISTURBANCES OF THE VASCULAR SYSTEM 

time a fluid rich in albumin, and thus capable of coagulation, escapes 
by the same route into the tissue (Fig. 10). This is called exudation. 
Some red corpuscles also escape through the walls (diapedesis) 
(Fig. 9, c). While inflammation involves an arterial hyperemia 
as its first stage and a venous hyperemia as its second stage, 
these two conditions are not necessarily inflammation, and may 
exist as entirely distinct conditions when produced by causes not 
leading to inflammation; also, it must be remembered that the results 
of venous hyperemia or infarction, e. g., extravasation, may lead 
to a subsequent inflammation. This does not make them identical. 
As the venous hyperemia of the inflammation increases, the flow 
of red corpuscles in the veins is increasingly retarded until stopped, 
when a to-and-fro motion (oscillation) begins. Finally all motion 
ceases, emigration ceases, and stasis is complete. This blood may 

remain fluid in the vessel for several days 
Fig. io (i. e., without coagulation), and if the 

blood flow be reestablished the separate 
red corpuscles are seen one by one to roll 
away from the general mass until all are 
in movement and stasis ceases. (Thoma.) 
Coagulation (thrombosis) may, how- 
ever, occur in the vessels involved in 
the stasis, and the part be later removed 
inflammatory edema of skin, through the process of resorption. (See 

The large spaces shown were . J; x . 

filled with exuded fluid, x -Resorption or Clot.) With the miiam- 
2.5. (Boyd.) mation fully established there are in the 

tissue the following elements: (1) Leuko- 
cytes and some red corpuscles and lymphocytes from the tissue 
lymphatics. (2) Coagulable lymph. (3) Later new embryonic cells 
formed by mitosis from preexisting connective-tissue cells which 
surround the leukocytes massed about the irritant. These are 
fibroblasts ready to form scar tissue — i. e., they are the elements 
composing granulation tissue. 
The disposition of these elements of inflammation is as follows: 

1. The leukocytes mass about the irritant, exert a certain amount of 
phagocytic activity (ferment action), and may in turn be injured, 
liberating thrombin, which, acting upon the fibrinogen of the lymph, 
produces fibrin, which in turn forms a coagulum (see page 25). 
This coagulum blocks the lymphatic vessels leading from the part 
involved, thus causing a retention of fluid in the tissue. This is the 
area involved in the stasis. 

2. In the later stages of non-infective inflammation the tissue cells 
undergo multiplication, forming cells larger and having more power 




INFLAMMATION 



39 



of ameboid movement and phagocytosis than the leukocytes. These 
become mingled with the leukocytes in the area of inflammation. 
They are fibroblasts from which all the connective tissues develop, 
and to the action of which regeneration is mainly due. The zone 
containing these elements is in a less degree of irritation and stasis 
and may be called the area of lesser inflammation. 

3. Around the area of lesser inflammation the bloodvessels are 
in a condition of arterial hyperemia, about this is an area of normal 
tissue. These areas shade off into each other. 1 



Fig. 11 




Acute bronchial catarrh: Passage of leukocytes through the epithelium of thehronchus 
between the ciliated cells. X 700. (Thoma.) 

4. The phagocytes cause dissolution of coagula and dead aseptic 
tissue, and remove them. If the irritant be thus removable it is eaten 
away and absorbed by the lymphatics. If the dead tissue be super- 
ficial, the connection with the living tissue beneath is thus dissolved 
and the latter sloughed off. If the superficial tissues have been pre- 
viously removed, the wound is covered with the exudates and leuko- 



1 Fig 13 serves to illustrate these areas, excepting the fact that the central area of 
pus is absent and occupied entirely by an area there termed stasis, as in this variety 
of inflammation pus is absent. 



40 DISTURBANCES OF THE VASCULAR SYSTEM 

cytes, which dry into a scab, beneath which regeneration occurs. If 
inflammation occur in a mucous surface, the exudate and corpuscles 
escape from the submucous tissue between the epithelial cells as a 
catarrhal discharge (Fig. 11). This may be due to infective causes. 
If the inflammatory exudate be highly coagulable and coagulate, firm 
swelling is caused, apt to lead to organization of tissue, hence called 
fibrinous inflammation. If it be productive of hypertrophy, it is called 
productive inflammation. This new tissue being hard it is termed 
induration. If the exudate be watery, poor in albumin, and hence 
not readily coagulable, the inflammation is called serous inflammation. 
In the later stages of simple inflammation the coagula are dissolved, 
the leukocytes undergo fatty degeneration, and both are absorbed, 
together with such tissue as has undergone liquefaction. The lympho- 
cytes and embryonic cells push into the area and regenerate the tissue. 
This is the phenomenon of resolution. 

Symptoms of Simple Inflammation. — These are: 

1. Redness due to the excess of blood in the vessels and in the tissue. 
In some cases the part may have a dusky hue. The color is deepest 
in the area of greatest stasis. 

2. Heat due to the increased oxidation in the area of hyperemia 
about the area of stasis. It has been shown that there is no increased 
heat in the area of stasis. In this area chemical action is lessened. 

3. Swelling due to the excess of blood in the vessels, the exudates 
of leukocytes and fluid, and the multiplication of tissue cells. The 
hardness of a swelling is due to coagulation of the fluid exudate. 

4. Pain. — The result of the pressure of the effusion upon sensory 
nerve terminals and their hyperesthesia (see page 34) ; it is frequently 
throbbing in correspondence with the heartbeat; the impulse causes 
temporarily increased pressure upon the nerve terminals. Gravita- 
tion also increases the pressure and pain in a dependent part — e. g., 
in a hand or foot or in recumbency in case of pulpitis (which see). 

5. Impaired function is an evident result of a disturbance involving 
such pathological phenomena as have been described. The part 
cannot be used owing to pain and stiffness due to the swelling, also 
nutrition of any part being impaired, it loses its normal function. 

There are certain adjunctive symptoms, such as hypercementosis, 
osteosclerosis, which are evidences of continued arterial hyperemia 
(see page 49) ; these results are mainly due either to arterial hyper- 
emia as such, or to the arterial hyperemia which is associated as an 
outer zone (or first stage) of all true inflammations (see Fig. 13). In 
like manner resorption of bone (osteoporosis) or tooth substance are 
associated with the zone of inflammation called lesser inflammation 
(see page 39) . It does not matter if the inflammation be of septic origin 



INFLAMMATION 41 

as there will always be these areas or zones outside of the septic area. 
In themselves these areas are to be practically regarded as aseptic 
and to be functioning under such conditions even though the central 
area be septic. 

There are no general disturbances in simple inflammation beyond a 
slight traumatic fever due to absorption of some aseptic material 
from the seat of inflammation — e. g., thrombin. 1 There may, how- 
ever, be general disturbance due to pain, loss of sleep, appetite, etc. 
Shock due to widespread inflammation, as from burns, may be 
serious. 

Infective Inflammation. — If microorganisms enter the tissue 
through a wound or puncture or an abraded surface, or invade a hair 
follicle, or if they locate upon predisposed or non-resistant mucous 
membrane, their multiplication causes irritation and inflammation of 
the tissue about them, probably a chemical effect of their enzymes. 
This at first resembles a simple inflammation, but later becomes 
more severe, prolonged, and may spread into the surrounding tissue, 
or in some cases cause inflammation in another place in no way 
connected with it except by the blood or lymphatic channels (metas- 
tasis). Briefly the process may be described as beginning with the 
entrance or location of the organisms and their multiplication. An 
injury of the vessel walls and degeneration of some tissue occur 
and the phenomena, such as occur in simple inflammation, begin. 
There is arterial hyperemia, later retardation of the blood current; 
emigration of leukocytes occurs, and a copious exudate of coagulable 
lymph is poured out into the perivascular tissue. This is supposed 
to be Nature's method of limiting suppuration, etc., to a limited area. 
By positive chemotaxis the leukocytes are attracted to the bacteria, 
surround them, and apparently endeavor to limit their activity, or, 
perhaps, to digest them. If the bacteria be few in number and not 
too virulent, the phagocytes are successful and the phenomena of 
resolution occur. If, however, the contrary be the case, the leuko- 
cytes are overcome and the inflammation spreads. In case of much 
toxin formation, negative chemotaxis occurs and phagocytic phe- 
nomena are held in abeyance. The central or most involved area dies. 
It is thus seen that there may be two terminations of an infective 
inflammation — resolution and necrosis. In certain cases what is 
termed subacute inflammation occurs as in arthritis, in which no 
necrosis beyond a possible molecular or cellular one (necrobiosis) 
may occur, though these are now attributed to bacterial action 
(especially for Streptococcus viridans) . What are termed plasma cells, 

1 "Green's Pathology and Morbid Anatomy. 



42 DISTURBANCES OF THE VASCULAR SYSTEM 

oval cells having power of phagocytosis, are found in the chronic cases. 
(See Granuloma for description.) 

Resolution. — If the phagocytes destroy or wall up the bacteria, 
so that they die in their own products or are killed by the protective 
juices of the part (alexins), the phagocytes undergo fatty degenera- 
tion, the lymphatics are unblocked by liquefaction of the coagulum, 
the circulation is reestablished, the tissue that has died is removed 
by resorption and replaced by scar tissue if the loss be considerable. 
No evident pus or externally evident necrosis is produced, and the 
part exhibits phenomena much like those of a simple inflammation. 
This is the only termination for a simple (non-infective) inflammation. 

Necrosis. — Death of a part may result from infective inflamma- 
tion, either with or without pus formation. 

Suppuration. — If the irritant in the tissue consists of pyogenic 
organisms, such as the Staphylococcus pyogenes aureus or albus, the 
Streptococcus pyogenes, the Bacillus pyocyaneus, Bacillus typhi 
abdominalis, Bacterium pneumonia?, or the gonococcus, pus will 
be formed, provided the germs be not killed. 

Entering a part, the bacteria distributed in the tissue act as irritants 
and excite the phenomena of inflammation as described. Some of 
the bacteria are taken up by the fixed connective-tissue corpuscles, 
the leukocytes, and the endothelial cells of the capillaries, and some 
lie free in the tissue. They multiply and the polymorphonuclear and 
eosinophile leukocytes increase in number by diapedesis and surround 
them. The original tissue cells, including those of the bloodvessels, 
undergo coagulation necrosis as the result of the action of bacterial 
ferments and do not take up staining reagents (Fig. 12). Coagulation 
of the exudates occurs. The leukocytes and tissue cells are in part 
degenerated into pus corpuscles by the action of the unorganized 
ferments of the bacteria — i. e., their nuclei are fragmented, and they 
undergo fatty degeneration. Some bacteria die. The exudate is 
peptonized into a fluid, which, together with the bacteria, dead 
leukocytes (pus corpuscles), and tissue remnants, constitutes pus. 
About this pus is a circumvallating wall of living leukocytes (area of 
stasis, Fig. 13), and about this again a zone of fibroblasts arranged 
about new capillary loops (granulation tissue), leukocytes are abun- 
dant and circulation more free (area of lesser inflammation). The 
whole constitutes, when confined within tissue, an abscess. When 
upon a surface the area of stasis, etc., is upon the under side only, 
the whole constitutes a suppurating ulcer. 

While the leukocytes may overcome the bacteria, the reverse is 
often the case, and the pus cavity enlarges in the same manner as at 
first by a new formation of coagulation necrosis, more circumvallation, 



INFLAMMATION 



43 



further liquefaction of the coagulum, etc. The path offering the least 
vital or mechanical resistance is usually followed until the surface of 



Fig. 12 




Miliary abscess in a case of septic embolism of the kidney: a, leukocytes advancing 
toward and surrounding (6) a mass of cocci, in whose neighborhood all trace of struc- 
ture has disappeared; c, renal epithelium too damaged by bacterial products to take 
the stain; d, kidney tissue staining normally; e, vein from which leukocytes are 
making their way to the commencing abscess. X 100. (Green.) 



the body or some internal cavity is reached. The last portion of 
tissue overlying the forming pus is tumefied and a soft, yellow spot 
appears. This is called pointing. The tissue is ruptured by the 



44 DISTURBANCES OF THE VASCULAR SYSTEM 

internal pressure and the pus escapes. The tract from the point to the 
abscess cavity is a fistula or sinus. As soon as this occurs granulation 
tissue springs up upon the sides of the abscess cavity and usually 
soon fills it with scar tissue. (See Regeneration.) If the cause con- 
tinues to act, as, for example, in case of a portion of dead and septic 
bone beneath soft tissue, a gangrenous pulp in a tooth root or infected 
crypts of the abscess walls, the granulation tissue continuously breaks 
down, and the condition is one of ulceration or a chronic abscess with 
a fistula. If, in the course of abscess formation, bone be encountered 
by the pus, it may be and often is molecularly broken down into pus 
(see Acute Apical Abscess), or the medullary tissue alone may be 
liquefied (osteomyelitis forming caries of bone), or a considerable 
portion of bone may be included in a profound surrounding inflamma- 
tion, die and be sequestered. (See Necrosis of Bone.) It does not 
always happen that the pus finds escape either naturally or through 
surgical aid; the patient may die before this occurs, or the tissues 
around the seat of pus formation may form a boundary wall which 
the bacteria fail to break down and thus die starved out. The abscess 
contents may undergo changes resulting in caseation, or later the mass 
may calcify. In tubercular caseations the tubercle bacilli may live 
for a long period. The Streptococci pyogenes may multiply laterally, 
following the subcutaneous cellular tissue, and produce violent 
spreading inflammation with but little pus formation — e. g., some 
forms of apical abscess and erysipelas. 

The products (toxins) from an abscess or infective inflammation 
may find their way into the blood, and a general toxemia result, or the 
bacteria themselves may enter the blood and a general infection 
result (septicemia). There are various varieties of pus which have 
names describing the chief characteristics : 

Creamy pus is the so-called laudable pus associated with an acute 
abscess or ulcer which progresses, as a rule, toward a cure. It is of 
a yellowish-white color, creamy consistency, and without much odor. 
Some surgeons prefer that this occur in certain conditions as being 
a sign of circumvallation by the defensive living parts and a lique- 
faction of the tissue containing multiplying bacteria not readily 
removable by anything short of ablation. 

Curdy pus contains flakes. 

Ichorous pus is thin, odorous, and irritating. 

Mucopus is pus containing mucus. 

Seropus is pus containing much serum. 

Sanious pus contains blood. 

Symptoms. — The symptoms of suppuration are both general and 
local. 



INFLAMMATION 



45 



Local Symptoms. — The symptoms of inflammation — redness, heat, 
pain, and swelling — occur, but usually much aggravated. The pain is 
often of a lancinating character, sudden darts often following com- 
parative quiescence. On the other hand, the throbbing pain may 
be continuous and intense, especially when the pus is confined by bone 
or tense tissues, as in the case of a felon or an acute apical abscess. 
Recalling that around the pus area there is an area of stasis, next one 
of active but lesser inflammation, and about that hyperemic, then 
normal tissue (Fig. 13), one may judge of the degree of involvement 
of deeper parts by the appearance of the surface above them. Thus, 
for example, hyperemia at the surface indicates inflammatory action 
directly beneath, with a pus cavity still deeper, while inflammation 




An abscess in the skin. The horny layer has largely disappeared, and the Malpig- 
hian layer is pushed upward by the subjacent abscess (a). The mass of pus corpuscles 
is just breaking down to form a cavity (P), the walls of which are thickly infiltrated 
with similar cells or the area of stasis (S). Outside is the area of lesser inflammation 
(LI), and still farther away are the areas of arterial hyperemia (H) and normal tissue 
(N.T). Interpretation modified by editor. (Boyd.) 



at the surface, together with hardness and tumefaction, shows a more 
involved condition of the tissue directly beneath it — i. e., a more 
advanced state of inflammation or even of suppuration. 

The softening of the apex of the swelling gives a feeling of lessened 
resistance, indicating pointing or pus at the surface. In large, super- 
ficial abscesses the sensation known as fluctuation may be obtained by 
placing one finger on one side of the swelling and gently tapping upon 
the other. Yellowness of the apex, together with softness, indicates 
that the abscess is about to discharge its contents. A fistula or sinus 
upon the surface is indicative of a discharged abscess, and leads to the 
pus-forming area beneath (chronic abscess). The symptoms will be 
modified by the anatomy of the part. In the case of the teeth adjunc- 



46 DISTURBANCES OF THE VASCULAR SYSTEM 

tive symptoms are valuable and will be considered in detail. (See 
Pulp Diseases or Pericementitis.) The adjunctive symptoms referred 
to on page 40 should here be considered. 

General Symptoms. — If toxemia be produced there may be chills, 
and, at the same time, fever as high as 104° F. A full, bounding pulse 
accompanies this, the patient is constipated, has a coated tongue, is 
exhausted by loss of sleep and appetite and often disturbed nutrition 
due to the pain. There may be other evidences of septic intoxication, 
such as recurring rigors (chills), pallor, nausea, vomiting, headache, 
diarrhea, a fluttering weak pulse and clammy extremities, with 
increasing debility, which indicates toxic effects which call for surgical 
eradication of pus foci and blood antiseptics. Thus, for example, 
an abscess on a lower molar developing swelling in the submaxillary 
region without development upon either side of the gum and asso- 
ciated with the said symptoms of debility, calls for extraction, local 
disinfection and drainage and blood antiseptics, such as mercuric 
chlorid, ferric chlorid, hexamethylenamin, etc., to which reference will 
be made in place. (See Index.) 

Leukocytosis after surgical disease is considered pathognomonic 
of suppuration, the count running up to 15,000 or 20,000 or more 
per cubic millimeter. (See page 23.) 

The logical conclusions of a case not recovering from a local infec- 
tion are : 

1. An acute toxemia. 

2. An acute septicemia. 

3. A chronic toxemia or septicemia which may be a combination 
of both. 

Ulceration. — This is a loss of epithelial surface extending into the 
corium. The development of microorganisms upon a free surface 
causes tissue degeneration and death, as described on. page 41. 

Numerous forms of pathogenic organisms are capable of causing 
tissue degeneration and death of a mucous or skin surface. If infec- 
tion take place through a hair follicle, or if organisms develop upon an 
abrasion, or in the epithelium in conditions of general or local debility, 
the epithelium is destroyed over an area, and in the subepithelial 
tissues the organisms multiply and cause tissue loss. If the organisms 
be pyogenic — and ulcerous surfaces are usually infected by these 
bodies — pus is formed (Fig. 14). Under some conditions, as in 
debilitated and neglected children, the ulcerous process may spread 
rapidly, as in the cheek in cancrum oris; or when specific bacilli, 
which excite much swelling and quick death of the tissues of the 
cheek, proliferate, causing the condition called noma. (See Index.) 



INFLAMMATION 



47 



Acute Toxemia. — The poisons, theoretically, may alone invade the 
blood, producing in some diseases death by intoxication (action on 
body cells in general), e. g., tetanus or diphtheria. 

Acute Septicemia. — The bacteria, and the toxins usually as well, 
enter the blood, produce a clumping of red corpuscles at certain 
points in the capillaries, develop in the local focus, and spread their 
toxins through the system; the spleen is usually enlarged, the red 
corpuscles disintegrated, the lungs congested and the heart finally 
fails. The symptoms of debility given on page 46 are followed by 
delerium, coma and death. 



Fig. 14 




Tuberculous ulcer of the intestine: a, mucosa; I, submucosa; c, muscularis ; g, ulcer; 
t, tubercle in the mucosa; t', focus caseating in the middle. X 12. 



Pyemia. — This is a modification of septicemia in which pyogenic 
organisms from some original focus locate at many points forming 
multiple abscesses, which interfere with local function, act as foci 
of further infection (metastasis) and toxemia and almost invariably 
produce death as in septicemia; occasionally it becomes chronic. 

Chronic Infection. — Certain bacteria developing in dental abscesses, 
pyorrhea pockets, the tonsils, the appendix vermiformis, etc., and of 
modified virulence seem to possess the power of forming either sup- 
purative metastatic infections, such as furuncle, appendicitis, arthritis, 
endocarditis or non-suppurative diseases representing an infection 
transferred from the original focus and which may be of chronic 
nature yet seriously endangering life through the secondary disease 
produced. This will be considered at length in a later chapter. 
(See Blind Abscess.) 



48 DISTURBANCES OF THE VASCULAR SYSTEM 

INFLAMMATION OF BONE. 

"Active inflammatory changes may occur in the periosteum, the 
medullary canal, the medullary spaces of the spongy bone, and 
the Haversian canals, the compact tissue and ground substance 
remaining passive." 1 The inflammation is termed periostitis, osteo- 
myelitis, or osteitis, the terms referring to the point of location of 
the inflammation — i. e., the periosteum, the medulla, and the spaces 
— the bone being involved in all cases. Inflammation of bone may 
be non-infective or infective; the latter is usually due to pyogenic 
organisms — i. e., suppuration occurs. 

Proliferative Periostitis. — This is a proliferation of cells of the 
deeper layers of the periosteum combined with emigrated leukocytes. 
A node is thus formed which may ossify. Practically it may, like 
hypercementosis, be regarded as a lesser inflammatory area (Fig. 13), 
an aseptic mild inflammation in which the area of hyperemia is the 
proximate constructive element. 

Suppurative Periostitis. — Pyogenic organisms may enter an 
injured periosteum or one weakened by previous disease (e. g., by 
scarlet fever). The origin of the bacteria is by way of the blood, 
either directly or by way of the medulla (as a secondary effect of 
osteomyelitis), or by way of the skin. It may occur as in a dental 
mucous anesthesia performed intraperiosteally with a septic needle. 

Pus forms beneath the periosteum, raises it, and destroys its 
connection with the bone. The vessels are stretched, damaged, and 
thrombosis occurs. Superficial necrosis of bone results, which may 
be total if other sources of blood supply are also cut off. 

Acute Osteomyelitis. — This is a suppuration occurring in the 
bone-marrow, which infects the bone proper, causes much throm- 
bosis of vessels, coagulation necrosis of bone cells, and may rapidly 
cause much necrosis of medullary tissue. Occurring in large bones, 
much toxin is produced, which may rapidly cause death. The organ- 
isms and thrombi formed, becoming emboli, may rapidly lead to 
pyemia. 2 Prompt surgical interference is called for. 

Inflammation of bone may lead to its rarefaction (rarefying 
osteitis or osteoporosis), its condensation (condensing osteitis or 
osteosclerosis), or its death (necrosis and caries). 

Rarefying Osteitis (Osteoporosis). — In the rarefying process 
which occurs in chronic inflammation, granulation tissue is formed, 
(for practical teaching purposes a more or less aseptic area of lesser 
inflammation), which enters the Haversian canals and spaces of 

1 Schmaus and Ewing, Pathology and Pathological Anatomy. 

2 Park's Surgery. 



INFLAMMATION OF BONE 



49 



Fig. 15 



spongy bone and destroys (resorbs) the bone, owing to the presence 
of osteoclasts. They thus form new channels between the spaces — 
perforating canal resorption (Fig. 15). When suppuration (ulcera- 
tion) is added by entrance of bac- 
teria, the granulations break down, 
leaving the bone as a dead, spongy, 
or honeycombed mass. This is 
caries of bone. In the early stages 
the inflammation may cease, and 
the bone not only be restored, but 
condensed. 

Condensing Osteitis (Osteoscler- 
osis). — In chronic inflammation, 
of lesser degree, instead of rarefac- 
tion, construction occurs and the 

trabecule of bone may increase in thickness, so that all spaces and 
Haversian canals become smaller. This is due to the area of arterial 
hyperemia, which for practical teaching purposes the writer asso- 




Trabeculae of bone with perforating 
canals. X 50. 



Fig. 16 



Fig. 17 




m : :r;--/ j m '" r %0< 




Section of bone and periosteum cover- 
ing it: B, bone; c, outer fibrous layer; 
a, inner layer of white fibrous tissue; O, 
layer of osteoblasts, some of which reach 
the bone with their prolongations. Nor- 
mal bone. (Black.) 



Section of bone and periosteum 
covering it: a, osteoclasts, cells that 
absorb bone; 6, surface of bone, 
showing fibers of periosteum pene- 
trating it and a Howship lacuna. 
Lacunar resorption. (Black.) 



ciates with Constructions. The bone becomes very compact and 
less vascular, and if built up in excess of its original dimensions, 
constitutes the condition known as exostosis; if very dense, as " ivory 



50 



DISTURBANCES OF THE VASCULAR SYSTEM 



exostosis." Both condensing and rarefying osteitis occur about the 
alveolar process and the roots of teeth. (See Hypercementosis and 
Resorption.) 

Resorption of Bone. — Under conditions of chronic inflamma- 
tion bone is often removed by neighboring tissue in one of several 
ways. 

Lacunar Resorption. — In this form the bone is excavated by giant 
cells into bays called Howship's lacunae, which may enlarge, or later 

a reconstructive action may 
Fig. is occur and osteoblasts may fill 

up the bays with bone. (See 
Fig. 17 and Resorption of 
Roots.) 

Perforating Canal Resorption. 
— This has been described un- 
der Osteoporosis. The canals 
connecting medullary spaces 
are enlarged by the granula- 
tion tissue formed in them 
(Fig. 15). , 

Halisteresis Ossium. — In this 
form of resorption the bone 
first undergoes decalcification and the matrix is later removed (Fig. 
18) . It occurs in conditions of osteomalacia, as in pregnancy, senility, 
etc. It also occurs in the alveolar process, and is, at least in part, 
the cause of the cleanly symmetrical resorption of the gum and 
alveolar margins. (Talbot. 1 ) 




Lattice-work figures in halisteresis. 
v. Recklinghausen.) 



(After 



NECROSIS. 

Necrosis (from nekros, dead) signifies, in its broadest sense, death 
of tissue. It is due to profound disturbance of its nutritional function 
or to direct injury to its elements. 

Necrosis proper (per se) signifies death of tissue in mass from any 
cause. 

Necrobiosis means the death of cells through the process of 
atrophy or degeneration, which are successive changes leading to 
death. It is also spoken of as molecular death of tissue. 

Necrosis of bone signifies the circumvallation and death of bone 
through the process of inflammation, which causes thrombosis of 
its vessels and cessation of its nutrition. The dead part, when 
separated, is called a sequestrum. The solution of continuity is 



1 Interstitial Gingivitis, 






NECROSIS 51 



effected by leukocytes massed about the portion in which nutrition 
has ceased. New bone, growing from the living bone, and inclosing 
a sequestrum is termed an " involucrum," a marked example occurring 
in phosphor-necrosis (which see). The necrosed portion is hard but 
may have undergone osteoporosis and when sequestered is movable ; 
usually a fistula forms. 

Caries of bone is that form of bone death in which the bone is 
honeycombed and molecularly broken down rather than seques- 
trated. (See Osteoporosis.) The part is not sequestered and is 
readily penetrated by a stiff, sharp probe; one or more fistula are 
usually present. 

Fig. 19 




Senile gangrene of the great toe, from a case of arterial thrombosis. The toe is 
shrunken and its epidermis is being exfoliated. At the line of demarcation the skin 
has retracted (a) and the deeper parts are separating (6). (Green.) 

Gangrene is a term used to signify death, en masse, of a part, 
through interference with its circulation, the hard parts being in- 
cluded. The dead part later undergoes drying or mummification (dry 
gangrene) or putrefactive softening (moist gangrene) under the action 
of bacteria. The death may occur through (1) purely circulatory 
disturbances cutting off nutrition, (2) through disease of controlling 
nerves or (3) through direct destruction by mechanical or chemical 
agents including the effects of bacteria. The dead part is sequestered 
by a zone of leukocytes as a " slough" or " sphacelus," which is thrown 
off. Strictly speaking gangrene occurs at the moment death of the 
tissue occurs and the tissue may at that moment be aseptic as in the 
case of a pulp going through venous hyperemia (q. v.). Therefore dry 
and moist gangrene are not strictly mummification and putrefaction 
though these later ensue. The dry form is due to stoppage of the 
artery causing ischemia, the moist form to stoppage of the vein 



52 DISTURBANCES OF THE VASCULAR SYSTEM 

causing venous hyperemia. Bacteria entering the dead portion may 
infect and involve the surrounding tissue in a "spreading gangrene" 
or the living tissue may establish a line of demarcation consisting 
of protective leukocytes, which dissolve the connecting tissue and 
separate the dead portion, as in the case of sequestered bone. The 
dead portion so separated is called a "slough" or "sphacelus" This 
is "circumscribed gangrene" 

In the aged atheromatous or calcareous changes in the arteries 
produce a slow circulation in the extremities. A slight injury to a 
vessel wall may induce extensive thrombosis (which see) . The result 
is gangrene of a part or all of an extremity, known as senile gangrene 
(Fig. 19). 

Necrosis may be of several types, of which the following are the 
chief forms: 

Coagulation Necrosis. — When a dying tissue contains coagulable 
material and the necessary ferments, the parts undergo coagulation. 
(See Coagulation.) The cells and parts about become solidified, the 
cells lose their nuclei and do not stain as usual, and the part appears 
glazed, pale, and waxy. It occurs in suppuration, and is due to the 
coagulating ferments of pyogenic cocci. (See Bacterial Ferments; 
also Fig. 12.) 

The thrombosis of the vessels about an area of infective inflam- 
mation is probably due to the same ferments. 

Fat Necrosis. — This is a peculiar form of fat death in which the fat 
is split into glycerin and fatty acid by lipase (a ferment). The fatty 
acid remains and combines with inorganic salts. 

Liquefaction Necrosis. — This is the death of tissue with liquefaction 
of the proteid material in the area, which is usually rich in exudates. 
The process is probably due to enzymes capable of liquefying the 
tissue. 

Necrobiosis, Necrosis Proper, Gangrene as described. 

REGENERATION OF TISSUES. 

Connective tissues that have been lost by inflammatory process or 
surgical operation are replaced by granulation tissue arising by mitotic 
division of cells of the connective-tissue group. The forms of healing 
are (1) by first intention, (2) second intention or granulation, (3) 
healing under a scab, (4) healing under a clot. Epithelial tissues are 
replaced only by multiplication of epithelial cells. The forms of heal- 
ing are practically alike by formation of granulation tissue, the form 
being simply a modification (of extent) of healing by second intention. 
This granulation tissue is transformed into fibrous tissue, the original 



REGENERATION OF TISSUES 



53 



tissue rarely being reproduced to any great extent though bone may 
be regenerated. (See Apicoctomy, Apical Abscess, etc.) 



Fig. 20 




Regeneration of capillary bloodvessels: a, normal capillaries; b, capillary process; 
c, new capillary appearing in divided process; d, process undergoing division; e, con- 
necting cell in which no sign of division has yet appeared. Diagrammatic. (Green.) 







A granulating surface: a, layer of pus; b, granulation tissue with loops of blood- 
vessels; c, commencing -development of the granulation tissue into a fibrillated struc- 
ture. X 200. Diagrammatic. (Rindfleisch.) 



54 



DISTURBANCES OF THE VASCULAR SYSTEM 



Healing by Second Intention or Granulation. — Shortly after evacu- 
ation of pus from an abscess the process of repair is instituted. The 
leukocytes come to the surface of the wound in great numbers, an 
exudate of lymph also occurs; some of these may degenerate into 
pus cells. Immediately beneath the uninjured connective-tissue cells 
multiply, forming embryonic cells (fibroblasts) ; at the same time the 

Fig. 22 




Transverse section of granulation tissue from an open wound with fibropurulent 
deposit: a, granulation tissue; b, fibropurulent deposit; c, c, bloodvessels. X 150. 
(Ziegler.) 



endothelial cells of the capillaries multiply at points, throwing out 
solid-pointed projections or buds from the sides of the capillaries 
Fig. 20, b). These lengthen and join buds from other capillaries 
(Fig. 20, c, d, e). By mitosis the nuclei divide horizontally, lying side 
by side (Fig. 20, d). Later these separate into two cells, discovering 
a lumen into which blood enters from the parent capillary (Fig. 20, 



REGENERATION OF TISSUES 



55 



a', c). In this manner loops are formed, about which the fibroblasts 
are arranged (Figs. 21 and 22). 

Together these form minute red elevations upon the surface of the 
abscess cavity or wound, called granulations. Repeated, the process 
gradually fills the abscess cavity. 

Naturally, collapse of the walls or apposition of cut edges of a 
wound lessens the amount of granulation tissue necessary; hence, in 
the latter case, healing by first intention (with a minimum amount 
of granulation or scar tissue) . Even in a cut with the edges constantly 
moved, as on the tip of a finger, the area is gradually obliterated by 
second intention. 

Fig. 23 




Laparotomy wound — sixteenth day: a, a, epithelium; 6, 6, corium; c, subcutaneous 
fat; d, vessels in scar tissue of corium; e, newly formed epithelial layer; /, vessels in 
subcutaneous scar tissue. X 40. Modified from Ziegler. (Green.) 



The wound having been filled up, epithelium grows from the sides 
and covers the granulations (Fig. 23, e). The granulation tissue, at 
first highly vascular, later contracts, and many vessels are obliter- 
ated so that it becomes whiter than normal tissue — cicatricial tissue 
(scar tissue) . 

The indifferent embryonic cells may have the function of forming 
any of the connective tissues. If cartilage is to be formed, chondrifi- 



56 



DISTURBANCES OF THE VASCULAR SYSTEM 



Fig. 24 



cation takes place about the specialized cells. If bone is to be formed, 
certain cells form islets, about which calcification proceeds. Nerves 
require a month or more to pierce the cicatricial tissue (Eichhorst). 1 
In spite of this assertion the writer finds that granulations are very 
sensitive to touch, which seems clinical evidence of error in this 
observation. 

In healing beneath a scab the exudation and leukocytes upon the 
surface of the wound dry into a scab beneath which granulations 

and an epithelial covering are 
formed. Later the scab falls 
off, usually being lost first at 
the periphery as the epithelium 
is formed. If prematurely lost 
the granulations are exposed 
and the smooth new epithelium 
disclosed around the central 
area of granulations. 

In healing wider a clot the 
clot is invaded by leukocytes, 
which have a solvent action 
upon it. Granulation tissue 
forms upon all sides of it, grows 
into it, and, at the same time, 
removes it by resorption (Fig. 
24). If the clot become septic 
the granulations may become 
infected and break down, as 
scar tissue in its early vascular 
stages is of but feeble resistive 
power, though it does not ab- 
sorb toxins. (Park.) 

Healing under a clot is the 
form commonly seen after tooth 
extraction. While a clot is the 
best occupant of the alveolus, 
affording a scaffold for the granulations, if the walls are not infected 
(at least to the point of tissue death), granulations will usually fill 
it up or nearly do so. (See Dry Socket.) It is an interesting point 
that the alveolus is finally filled with bone, while the original bony 
margins of the alveolus are resorbed. 

In certain cases of abscess with contracted fistula? or openings of 




Absorption of blood clot. Section through 
the margin of a clot formed among the tissues 
by extravasation, showing the growth of 
granulations by which it is removed: a, a, 
portions of clot; 6, b, original tissue; c, c, 
granulations springing from the original tis- 
sue and projecting into the clot; d, d, wan- 
dering cells or leukocytes that seem to have 
taken red blood disks into their interior. 
(Section cut in gum arabic and stained with 
hematoxylin.) X 350. (Black.) 



Ziegler, General Pathology. 




DEGENERATION 57 

discharge, the orifice may close before the granulations have filled 
the pus cavity. If pus or an excess of exudate be now formed within 
the cavity, a second discharge may occur. To obviate this difficulty, 
abscesses are often packed with antiseptic gauze, so that healing may 
occur from the bottom of the cavity while drainage is resumed. In 
other cases the placing of a tent or drain tube in the fistula suffices. 
In other cases, as in bone cavities, semisolid substances such as 
Beck's bone paste or bone wax (q. v.) are introduced to occupy the 
cavity and exclude infective and foreign material while granulations 
form about it and gradually absorb it. 

DEGENERATION. 

Degeneration signifies a retrograde process in cells in which abnor- 
mal cell changes occur in consequence of disturbed nutrition. The 
cells usually gradually die after marked changes in their histology. 
This form of death is called necrobiosis. The tissue, as a whole, is 
still living. 

Fig. 25 Fig. 26 






. •••*«vr. * 



Liver cells in various stages of Fatty degeneration of cells: a, from a 

fatty accumulation. X 300. cancer; b, from the brain in chronic soften- 

(Rindfleisch.) ing. X 200. (Green.) 

Fatty Degeneration. — True fatty degeneration, also called fatty 
metamorphosis, is chiefly characterized by the presence of fat droplets 
within the cells and formed by conversion of the proteid into fat; it 
differs from fat infiltration in that in the latter fat enters the cells 
from without, and is a more or less physiological process (Figs. 
25 and 26). The greater the amount of fat in true fatty degener- 
ation the nearer the cell is to death. After its death it is probably 
absorbed. This condition frequently occurs in inflammations 
(Fig. 26). 

In areas which have undergone fatty degeneration a cheesy sub- 
stance may be formed out of the degenerated elements existing 
in the part. The fluid is gradually absorbed and a mass composed 




53 



DISTURBANCES OF THE VASCULAR SYSTEM 



of atrophied cells, fatty debris, and cholesterin crystals is left. This 
process is known as caseation (Fig. 14, t'). Encapsulation of the 
caseous mass by fibrous tissue may take place, or its liquefaction or 
its calcification may occur. Fatty degeneration may occur in many 



Fig. 27 




Fatty degeneration of the heart, from a case of pernicious anemia. The protoplasm 
is replaced by globules of various sizes stained black by osmic acid. The outlines of 
the fibers are irregular, owing to inequality in their distention. X 400. (Green ) 



Fig. 28 



tissues, and the danger is proportionate to the importance of the 
tissue involved. 

Various other forms of substances appear in cells degenerated by 
various causes, such substances give the designations — amyloid, 

mucoid, hyaline, fibroid, col- 
loid degenerations. The ap- 
pearance of glycogen in the 
cells has not been success- 
fully classified as either posi- 
tively a degeneration or infil- 
tration (Figs. 28 to 30). 

Cloudy Swelling (Parenchy- 
matous or Granular Degener- 
ation). — Cloudy swelling is a 
change occurring in the pa- 
renchyma (essential cells) of 
a part as the result of the 
presence of toxic substances in the blood, or even as the result of 
aseptic disturbance of nutrition, such as a severe burn. The same 
causes which produce fatty degeneration may produce it. 




Hyalin degeneration of small vessels in the 
cord. X 350. 



MGENERATION 



59 



Pathology. — The cell absorbs fluid, swells, its contents become 
granular, and the histological structure is lost. In the early stages 
the change is albuminous; no fat is demonstrable; later, however, 



Fig. 29 




Colloid cancer, showing the large alveoli, within which is contained the gelatinous 
colloid material. X 300. (Rindfleisch.) 



Fig. 30 







a~- --;&:>•• * Vr;- / 







i 



Cloudy swelling of kidney epithelium: a, normal epithelium; b, epithelium begin- 
ning to be cloudy; c, advanced degeneration; d, cast-off degenerated epithelial cells. 
From a preparation which had been treated with ammonium chromate. X 600. 
(Ziegler.) 



00 



DISTURBANCES OF THE VASCULAR SYSTEM 



it appears, so that the change is regarded as a first stage in the pro- 
duction of fatty degeneration, by which process many of the cells 
are lost, though the organ may recover if the patient withstands 
the original disease (Fig. 30). 



Fig. 31 




Adipose tissue: A, normal; B, atrophic, from a case of phthisis; a, single fat cell, 
with cell wall, nucleus, and drop of fat. X 300. (Virchow.) 



FlG - 32 Atrophy. — If hyponutrition be 

marked, the waste in a previously 
normal part may exceed repair, 
and the part affected becomes 
diminished in size or atrophied 
(Figs. 31, B, and 32). Atrophy 
may be general or local. In 
general atrophy there is a gen- 
eral loss of tissue, due to an 
excessive waste or faulty assim- 
ilation of food by the tissues'. 
There is a loss of body weight, 
due first to a loss of the fat, later 
to shrinkage in the tissue cells. 
The shrinkage in size of the tis- 
sue cells causes shrinkage of the 
entire organ. The cells and fat 
may recover their size when the 
faulty waste or assimilation is 
corrected. During atrophy many 
cells are lost through the process 
of fatty degeneration and re- 
moved by the phagocytes (leuko- 
cytes), so that atrophy may, like hypertrophy, be both simple and 
numerical. An atrophied part is pale and shrunken, contains less 
fluid, and is tough and fibrous. At times the fibrous portion or 
connective tissue may increase as the cells diminish (sclerosis). 
Practically fibroid degeneration is of this character (which see). 




Muscle fibers in simple atrophy. 
(Schmaus.) 



DEGENERATION 



61 



Causes. — General atrophy is caused: 1 (1) By a deficient supply 
of food material delivered to the tissue cells. This may be due to a 
primary food deficiency or any interference with its preparation for 
absorption or with its proper absorption or circulation. (2) By 
excessive waste of the tissues generally, as in fevers, prolonged 
suppuration, etc. (3) By impaired vital activity of the cells them- 
selves, as in senile conditions. 




Calcareous infiltration of renal epithelia. From the edge of an old infarct; 
tubules still to be recognized. X 250. (Schmaus and Ewing.) 



a few 



Local atrophy may be caused: (1) By a lessened circulation in 
a part due to obstruction of the arteries, veins, or capillaries, as, 
for example, by pressure (see secondary dentin). (2) By diminished 
functional activity or disuse of a part, as in the case of unused muscles 
or even bones. Certain organs are atrophied or resorbed as a part 
of the cycle of life, e. g., the umbilical cord, the roots of deciduous 
teeth, the thymus gland, the mammary glands after the menopause. 
(3) The loss of nervous connection of a part with the nerve centers 
controlling it (trophoneurosis), or through interference with nervous 
centers having trophic influence upon a part. (4) Excessive functional 
activity may cause atrophy by producing a degenerative condition 
due to overstimulation. 

Infiltrations. — An infiltration signifies the entrance into cells of sub- 
stances from without. Thus fatty, pigmentary, serous, calcareous 
and possibly glycogenic infiltrations are classified; of these the most 
interesting are the pigmentary (see page 78) and the calcareous. 

1 Green; Pathology and Morbid Pathology. 



62 DISTURBANCES OF THE VASCULAR SYSTEM 

Calcareous Infiltration. — In tissues which have undergone pre- 
vious degeneration, calcium, sodium, or magnesium salts may be 
deposited as an infiltration from the blood plasma. The parts are 
thus petrified. The cells take no active part in the process. 1 

It is believed, however, that the deposit of salts in the dying tissue 
is more than a mere precipitation,. arid that calcification results from 
a combination of the salts with an albuminous base and with fatty 
acids, such an affinity being favored by the degenerative changes. 
Ordinarily, the carbonate and phosphate of calcium are the infiltra- 
ting salts, but in gout uric acid salts are deposited, owing to an excess 
of uric acid in the form of biurates and quadurates in the body fluids. 
A sluggish circulation in the part favors the deposition of the salts. 
The calcification may occur in both the cells and in the intercellular 
substance. 2 (See Calcific Degeneration of the Pulp.) In the early 
stages the salts are found as fine granules in the intercellular substance. 

"The white, fibrous tissue is the form of connective tissue usually 
affected, but concretions may occur in the connective tissue sur- 
rounding the bloodvessels." 3 

As a secondary process after degeneration, calcification of the 
middle coats of the arteries may occur, rendering them inelastic. 
This renders them incapable of regulating the blood supply to parts, 
and these suffer more or less nutritive disturbance, and, in some cases, 
actual death of the part (gangrene). Calculi are found in tumors at 
times. Many forms of free calculi are formed in the body. These 
occur most frequently in ducts or cavities lined with epithelium, 
e. g., the salivary ducts and the bladder. 

"All free concretions have an organic basis or nucleus," with 
which are combined the calcium salts, oxalates, cholesterin, etc., 
making up the inorganic or crystallizable part of the combination. 
The organic part may consist of inspissated feces, as in enteroliths, 
globulin or possibly mucin, as in the calculi upon the teeth; epithe- 
lial scales, mucus, etc., in the urinary passages. 4 The fine crystals or 
granules are probably soluble in some cases. The larger calculi are 
probably permanent and cause degeneration of adjacent tissue. 

Calcareous infiltration is clearly to be distinguished from the 
normal calcification of the hard tissues, bone, enamel/ dentin, and 
cementum. These are composed of calcoglobulin, in which calcium 
and magnesium salts are combined under the superintendence of 
certain living cells with albuminous bases derived probably from 
their own substance. Black's theory of calculus formation (which 
see) may possibly be applicable, for if calculus exist in globules in the 
blood it could readily be deposited in any tissue. 

1 Green, Pathology and Morbid Anatojny. 

* Ziegler, General Pathology. * Ibid. 4 Ibid. 



SECTION II. 

ABERRATIONS IN ERUPTION OF THE TEETH. 



CHAPTER III. 

DENTITION: ITS PROGRESS, VARIATIONS, AND 
ATTENDANT DISORDERS. 

The process of teething, eruption, or dentition comprises that 
series of vital operations which causes the teeth to leave their crypts 
in the maxillse, to pierce 

the gum, and to take their Fig. 34 

places in the dental arches. 
It is a continuation of the 
process of dental develop- 
ment, and is accompanied 
and succeeded by root, al- 
veolar, and maxillary de- 
velopments, which are also 
to be considered in con- 
nection with it. 

Physiologically, denti- 
tion is divided into (1) 
the first dentition, or that 
of the temporary teeth, 
and (2) the second denti- 
tion, or that of the per- 
manent teeth. 

Examination of Fig. 34 
will show the state of 
tooth development at a 
period shortly after birth 

(a central incisor being under consideration). The crypt is roofed 
over at birth by a membranous structure. During the period from 
then to perhaps six months after birth, about one-third of the root 

(63) 




Developing tooth at birth: A, developing bone; 
B, tissue reflected from follicular wall and forming 
alveolar periosteum ; C, follicular wall; D, vessels 
and nerves; E, epithelium of gum. 






64 



DENTITION 



will have been formed and the tooth crown and part of the root will 
have extruded from the crypt and be merely covered by the soft tissues. 
(See Fig. 36.) The root end is widely open (incomplete) and the margins 
are thin and sharp. The vascular pulp and follicular tissue occupies the 
space between the root and the bone, and fills the interior of the root. 



Fig. 35 



22 months after birth 
18 months after birth 

12 months after birth 



6 months after birth 

40th week (birth) 
30th week embryo 
18th week embryo 
17th week embryo 




Calcification of the deciduous teeth. (Peirce.) 



Fig. 36 



Meanwhile the crown cusp will have advanced from the situation 
shown in Fig. 34 to a point just beneath the mucous membrane, 
which is pressed up and stretched over the advancing tooth crown, 
presenting to oral view a tumefied condition more or less correspond- 
ing to the form of the crown. 
This is nicely shown in Fig. 36, 
A and B. 

These anatomical data serve 
for the consideration of the 
causes and process of eruption. 
Causes of Eruption. — It is 
evident that there are forces 
which can bring about the 
elevation of a tooth crown from 
its bed in the crypt to its posi- 
tion in the mouth. 

The consideration of these has 
led to the development of the 
following rational theories, as 
well as others now obsolete: 
1. That crown elevation is due to the lengthening of the root — 
i. e., as root tissue is formed by the pulp and follicle wall lying beneath 
and to the side of its edges, the tooth is mechanically pushed up, the 
tissues lying above it are stimulated and absorbed, and as more root 
is formed, a further extrusion occurs, It is to be noted that the root 




Lines of incision in lancing: A, A, over 
the molars; B, B, over the cuspids and in- 
cisors before eruption; C, C, C, over the 
molars and cuspids after partial eruption. 



DENTITION 



65 



end occupies the same level, at all stages of eruption, in the devel- 
oping jaw that was occupied by the cervical edge of the crown 
(Fig. 37). As no two bodies may occupy the same space at the same 
time, the root-forming pulp and follicle wall push the tooth up, to 
gain room for more root formation. The mild continued pressure 
is quite competent to do this. The pressure of the soft tissues against 
the root end is explained by Constant to be derived from the normal 
blood pressure. 1 That such an internal pressure exists is shown by 
the extrusion of ordinarily confined parts when released from the 
accustomed pressure. A simple accident demonstrated this to the 
editor. While excavating with a large bur, the softened dentin about 
a decayed pulp chamber, the cementum was widely removed from 
the pericemental tissue beneath, which latter fortunately remained 
unbroken. It immediately protruded into the perforation. Constant 

Fig. 37 




Diagram showing the upward movement of the crown during eruption and root 
development. (Constant.) 



also cites the extrusion of a tooth in pericementitis as an evidence 
of the influence of the blood pressure. Another evidence is the 
occasional rapid advance of a tooth after lancing of the gum. 

2. The process of tooth development is a vital process, and that of 
eruption has been held also to be. (Tomes.) That cells concerned 
in development seem to have a predestined end or function cannot be 
denied; at the same time, throughout dental development, defined 
resistances to opposing forces seem to play a part in the moulding of 
the soft and hard tissues — e. g., the depression of the enamel organ 
by the papilla. 

3. Peirce 2 holds that the impact of blows upon the jaws causes the 
tooth to rise toward the gum. He explains the eruption of crowns 
without roots upon this theory. 



1 International Dental Journal, June, 1903. 
5 



American System of Dentistry. 






66 DENTITION 

4. Tomes explains the eruption of teeth, after development of the 
root, upon the theory that the closing in of the alveolar process or 
contraction of the alveolus upon the pericementum (follicle wall) 
causes the lifting up of the tooth. That such a closure occurs about 
the extruding roots of teeth left after the breaking away of the crowns, 
is shown by examination of the sockets of such roots. An abnormally 
shallow alveolus closed by deposition of bone at its apex will be found 
in cases of small apical portions of roots so extruded. 

It is well known that mild hyperemia is produced in pericementi 
which do not receive a normal resistance, which would account for 
both the elevation and bone deposition on the ground of blood 
pressure. (See Arterial Hyperemia.) 

Fig. 38 




Pulp cavities of the superior first bicuspid, from the seventh to the twelfth year. 

(BroomeU. 1 ) 

The Process of Dentition. — At varying ages, according to the 
state of tooth development, the formed crown of the tooth advances 
and presses upon the follicle wall overlying it; this is irritated, and 
giant cells are developed, which by resorption remove this as well 
as the upper edge of the wall of the crypt. In the anterior teeth this 
resorption occurs on the outer incisal half of the crypt wall, the inner 
side remaining intact (Broomell). The mucous membrane is pushed 
up and moulded over the crown, thereby causing a tumefaction. 

The mucous membrane, at first normal in color, becomes slightly 
hyperemic, and then may change to an ischemic condition and whiten, 
owing to the removal of the blood by the pressure of the underlying 
crown. Resorption from beneath causes a break in the continuity of 
the mucous membrane, and the crown tip erupts into the mouth 
(Fig. 36, C). 

The rate of resorption and crown advance are equalized in perfectly 
normal dentition. (See cause of pathological dentition page 70.) 

1 Anatomy and Histology of the Mouth and Teeth. 



DENTITION 



67 



The crown rises from the gum, is directed by the tongue and lip or 
cheek, and, finally, meets its antagonists of the opposite jaw. ' The 
interlocking of cusps and meeting of occlusal surfaces limit further 
movement of position. 

Meanwhile root development proceeds, and as it occurs the alveolar 
process is built about the pericementum, which consists of the follicle 
wall drawn up. By this means the roots are firmly implanted. 
The further development of 

the root proceeds until com- FlG - 39 

plete, and so remains until 
normal resorption of the 
temporary roots occurs, and 
for life in the permanent 
teeth. The scheme of root 
development and addition is 
shown in Figs. 38 and 39. 

The state of formation 
of the roots of temporary 
teeth at any given age may 
be judged by the table of 
averages shown by Peirce 
in Fig. 35. Being but aver- 
ages, allowance for precocity 
or delay must be made. 

Apart from the presence 
of the temporary teeth, the 
process of eruption is iden- 
tical in both sets of teeth. 
(Fig. 40.) 

Periods of Eruption. — 
As a general rule, the erup- 
tion of the deciduous teeth 
may be said to begin about 
the seventh month after 
birth, and is completed 

somewhere about the thirtieth month. Variations occur; some chil- 
dren may be born with teeth erupted; again, the initiation of the 
process may not occur until the twelfth month, or even later. 

The incisor teeth are usually erupted in pairs, the molars and 
cuspids making their appearance in fours, the first molars in one 
group, the cuspids in another, and the second molars in a third group. 
The several groups require different lengths of time to complete their 
eruption, the time occupied in the eruption of the first molars being 




Diagram illustrating root development and 
condition of an incomplete root: E, enamel; 
D, dentin; P, pulp containing odontoblasts, 
OB; AP, alveolar process; B, bone; C, cemen- 
tum; P', periosteum of bone continuous with 
the pericementum; PER, pericementum con- 
taining cementoblasts, CB; A, V, N, arteries, 
veins, and nerves. 






68 



DENTITION 



longer than that required for the eruption of the other groups. 
Between the appearance of additional groups of the teeth an interval 
elapses, no doubt a physiological provision, for, as will be shown 
later, the process of dentition is usually accompanied by evidences of 
more or less local disturbance, frequently by disturbances through- 
out the intestinal tract, and even reflex disorders of the central 
nervous system occur. It is believed, therefore, that the period 
which elapses between the eruption of the dental groups permits 
the organism to recover from the effects of previous disturbance 
before the new source of irritation appears. 

Fig. 40 




View of the upper jaw of a child, aged about six and one-half years. The anterior 
teeth are slightly separated by the partially developed permanent teeth, lying behind 
or posterior to them, pushing forward to occupy a more anterior position. The equal 
height which the crowns of the deciduous teeth originally occupied is also being dis- 
turbed by the advancing permanent teeth. (Peirce.) 

Table. 1 



Group 1 


Lower central in- 


Time of eruption, 


Duration of eruption, 


Interval, 2 to 3 months. 




cisors 


7 months 


1 to 10 days 




Group 2 


Upper central and 


Time of eruption, 


Duration of eruption, 


Interval, 2 months. 




lateral incisors 


9 months 


4 to 6 weeks 




Group 3 


Lower lateral in- 
cisors 


Time of eruption, 
12 months 






Group 4 


First molars 


Time of eruption, 
14 months 


Duration of eruption, 
1 to 2 months 


Interval, 4 to 5 months. 


Group 5 


Cuspids 


Time of eruption, 
18 months 


Duration of eruption, 
2 to 3 months 


Interval, 3 to 5 months. 


Group 6 


Second molars 


Time of eruption, 


Duration of eruption, 








26 months 


3 to 5 months 





1 Coleman's Dental Surgery (Stell wagen) . 



PATHOLOGICAL FIRST DENTITION 69 

In the above table it will be noted that the time of eruption of 
the lower lateral incisors is later than that of the eruption of the upper 
lateral incisors. The reverse course is frequently observed; indeed, 
it has usually been accepted as the rule of precedence in the United 
States. All tables, as to periods of eruption, give but the approxi- 
mate times; while variations are extremely common. The ages 
given in this table are those at about which the several teeth may 
be expected to make their appearance. Stellwagen (the American 
editor of Coleman), in commenting upon this table, states that the 
periods of eruption in this country are from one-seventh or more, 
earlier than the dates given. He suggests that the difference in 
food habit may account for the differences in time. 

Accompanying the development and eruption of the teeth, occur 
developmental changes in all of the glandular appendages of the 
alimentary canal; probably the alterations in their structure, and no 
doubt in their physiological chemistry, are accompanied by dental 
provision for the mechanical subdivision of foods of postinfantile 
character. 

Symptoms of Eruption. — Slight local disturbances are so com- 
mon in even so-called normal first dentition as to be accepted as 
physiological. The resorption of soft tissue around the tip of the 
crown of the tooth implies a condition of mild non-septic inflamma- 
tion at that point. In more marked cases there is evidence of some 
irritation cognizable to the infant; the gum is of a somewhat deeper 
color and its temperature is elevated. Relief is afforded by pressure, 
which temporarily reduces the hyperemia, and the child is pleased 
to have its gums rubbed, to bite upon its own or the nurse's fingers, 
upon rings or other objects. Still more marked is the soothing effect 
of biting upon cold substances, such as ice, which, in addition to 
mechanically lessening the blood supply, causes contraction of the 
dilated vessels. 

Slight reflex disturbances are evidenced by the stimulation of the 
salivary glands, which produces an increased flow of saliva. 

Reflex disturbances of more severe character occur in pathological 
dentition, to be considered later. 



PATHOLOGICAL FIRST DENTITION. 

The local disturbances may be exaggerated beyond that degree 
accepted as physiological, and may be accompanied by nervous, 
alimentary, pulmonary, or cutaneous disturbances. This is patho- 
logical dentition, and may be of several grades of severity. 






70 DENTITION 

Causes and Pathology. — The primary cause of pathological dentition 
may be stated as an inequality in the rate of gum resorption and 
crown advance. The advancing crown pressing upon the gum tissue 
causes irritation; the mild aseptic inflammation resulting, instead of 
remaining at a point favoring the development of giant cells and 
resorption, passes the physiological point and causes a disturbance 
of function. Inflammation, simple or even infective, may occur in 
the area. 

Swelling of the gum occurs, which, being distributed in all direc- 
tions, presses upon the crown, depressing it upon the pulp and follicle 
wall beneath the sharp root margins; at the same time the blood 
pressure of the tissues tends to press the tooth upward. The simple 
lack of resorption of the gum would be almost equally effective in 
preventing eruption and this may be an accompaniment of the 
inflammation (Impaired function, see page 40). 

The sharp edges of the root must irritate the sensitive and delicate 
pulp tissue, which becomes inflamed and swollen, and still more 
strongly urges the tooth upward. Two sources of disturbance now 
are possible: (1) the irritated gum tissue and (2) the irritated pulp. 
Though the pulp is more likely to produce the reflex disturbance, a 
gum inflammation, if intense, is often capable of producing even 
prostrating symptoms. (See Pathological Dentition of Third Molars.) 
Through the intimate sympathetic relations of the fifth cranial nerve, 
supplied to the pulp, with the sixth, seventh, ninth, and tenth cranial 
nerves in and about the floor of the fourth ventricle of the brain, 
salivary, muscular, nervous, alimentary, and pulmonary disturbances 
become possible. Any systemic disturbance — e. g., measles, general 
debility, or lesser disturbance, etc. — which lowers the general nutri- 
tive function also in the parts associated with the teeth, may favor 
the production of local pathological phenomena. Again, systemic 
disturbance readily produces a hyperesthesia of the nervous system, 
favoring the production of nervous phenomena. 

Pathological dentition may occur in the absence of an evident 
hyperemic gum tissue. The tissue may be white, showing ischemia 
from pressure, a binding down of the root end upon the pulp being 
proved by the subsidence of symptoms after lancing, and sometimes 
by the rapid, partial eruption of the tooth immediately after lancing. 

Again, pathological phenomena have been noted where no super- 
ficial local disturbance was evident. In these cases the deeper tissues 
may exert a restraining influence upon the crown, but the swelling 
is just as probable. 

It is to be understood that the nervous and digestive systems of 
the child are in a developmental condition, and therefore in unstable 



PATHOLOGICAL FIRST DENTITION 71 

physiological equilibrium, so that any added physiological work, such 
as unusual growth or dentition, may be more than the organism 
can endure without a definite loss of general vital potential. This 
may be further complicated by hereditary defects of tissue, such as 
neurotic, degenerative, or syphilitic taint, or conditions of hygiene or 
feeding tending to lower the health standard. 

Ottofy offers the following report, by the Bureau of Health of 
Manila, of 3250 deaths before twelve months of age : 

Before completing one month 647 

During second and third months 302 

Various causes not dental 959 

Four to twelve months due to convulsions and eclampsia . . . 1342 

Total 3250 

Showing a large number of deaths due to causes in which dentition 
may have been a determining or complicating factor. 

Dr. William P. Spratley, medical superintendent of an institution 
for epileptics, states it as his opinion that pathological first and second 
dentition is a determining cause of epilepsy in children having 
neuropathic taint in that direction. 1 

Symptoms. — The symptoms of pathological dentition are both local 
and general. 

Local Symptoms. — The local symptoms are usually those of inflam- 
mation, red and swollen gum tissues at times assuming a dusky hue. 
The gums may be white, and often glistening, indicating their tense 
stretching over the crowns. In the gum over the erupting tooth 
there may exist a vesicular enlargement containing fluid. 2 Evidence 
of local irritability is given by the fact that the child resists the 
touching of the gums, seizes the breast or bottle nipple, and imme- 
diately releases it. 

The readiness with which the child will take cold substances, ice 
or iced water, is notable and self-explainable. Alternate, excessive 
flow of saliva and oral dryness are present. 

In the more marked cases of local disturbance, evidences of bacterial 
infection of the mucous membrane of the mouth may make their 
appearance, such as ulcerative stomatitis. While, as a rule, the 
breaking down and ulceration of the tissue are confined to the parts 
overlying the erupting teeth, a general stomatitis or widely scattered 
patches of ulceration may make their appearance. 

General Symptoms. — The general symptoms may be differ- 
entiated into mild and severe. 

The mild symptoms are such as are attendant upon severe and 
painful inflammations about the face at almost any age; thus anorexia, 

1 Dental Cosmos, 1905. 2 Tomes, System of Dental Surgery. 



72 DENTITION 

fretfulness, anger, restlessness, sleeplessness, thirst, mild fever, and 
evident desire for the upright position occur. The pain is at times 
paroxysmal, but may become continuous. 

These symptoms subside upon the eruption of the tooth or lancing, 
though erupting cuspids, bound by a ring of tense gum tissue or by 
adjoining teeth, may continue the irritation even when apparently 
erupted (Fig. 36, C). Again, the cuspids may be caught between 
the lateral and first molar. The more severe general symptoms are 
such as are brought about by reflex neuroses. 

The roots of the fifth cranial nerves supplied to the teeth are in 
intimate relation with the roots of the sixth, seventh, ninth, and tenth 
cranial nerves in the floor of the fourth ventricle, as well as with 
other cranial nerves. It may be argued upon a priori grounds that 
irritation of the peripheral ends of the fifth in the pulp tissue may 
therefore readily produce neurotic results in the brain, salivary 
glands, skin, lungs, or larynx, intestinal canal, or muscles of the face 
or extremities. 

Taking the intestinal canal as the most complicated example, we 
find the following data: The stomach and intestines are under the 
influence of the pneumogastric nerve, which sends to its muscular 
coats both stimulant and inhibitory fibers. Likewise it sends vaso- 
motor fibers to the intestines, division of which leads to inhibition 
of the muscular fibers of the vessels and leads to vasodilatation 
and a great increase of very watery succus entericus. 1 

Intestinal Disturbances. — That intestinal disturbances may arise 
independently of teething is self-evident, but as they are most liable 
to so occur during the very period during which teething may be 
supposed to act as a primary cause of intestinal troubles; hence 
differentiation becomes important. 

As a rule, intestinal disturbances arise from improper feeding, the 
food acting as an indigestible irritant to the stomach and intestines. 
Even an excessive quantity of good breast or bottle milk may, if not 
regurgitated, act as an intestinal irritant. The milk of an excited, 
exhausted, or debauched nurse may also act deleteriously. Fermen- 
tation due to bacteria ensues, and diarrhea and colic are a natural 
result. Naturally uncleanly conditions concerning the milk, bottle, 
nipple, teething ring, etc., introduce an infective element which may 
be sufficient to this result. 

Musser 2 attributes these cases to development of the Bacillus coli 
communis and Bacterium lactis aeriformis existing harmlessly in the 
normal intestine, but developing under the abnormal conditions. 

1 Halliburton, Kirke's Physiology, 1896, p. 684. 2 Medical Diagnosis. 



PATHOLOGICAL FIRST DENTITION 73 

This occurring in warm weather, when the child suffers from 
intense heat, has a very debilitating if not fatal result, and may dis- 
turb all nutrition, including dentition, which, becoming pathological, 
adds its effects. In the so-called second summer the child often erupts 
cuspids or molars. 

A similar train of circumstances may be caused by teething. 
Peripheral irritation of terminals of the fifth nerve in the pulp may, 
through the tenth nerve, cause a reflex vasomotor dilatation in the 
walls of the intestines — i. e., hyperemia and excess secretion, a condi- 
tion which favors bacterial invasion. Intestinal digestion is dis- 
ordered, the vital resistance lowered, and an infection ordinarily 
resisted occurs, as when the intestine is primarily disordered. 

Diarrhea may follow. In either case alimentation is interfered 
with and the general nutrition suffers. The child is debilitated by 
lack of nutrition; moreover, toxic substances are generated in the 
intestine, which cause a toxemia, to which many of the general 
symptoms may be attributed, such as fever, meningitis, stupor, 
coma, and death. The general debility also further interferes with 
the process of dentition. Thus there may be a vicious circle. 

Diagnosis. — A diarrhea due to improper feeding would not be 
preceded by symptoms of pathological dentition, or may not occur 
at a time proper for dentition; would have a history of improper 
feeding, and possibly of unhygienic conditions, such as unsterilized 
milk or milk bottles, filthy surroundings, etc. There is a catarrhal 
diarrhea accompanied by vomiting and constant acid, watery stools. 
The stools may have a chopped-spinach character. There is colic 
due to collections of gas. 

Such an infective diarrhea may readily follow the reflex and 
debilitating effects of pathological dentition, as shown above. 

White 1 has noted that a choleraic diarrhea may accompany and be 
a sign of pathological dentition. Barrett 2 states that a diarrhea due 
to dentition will probably be followed by constipation. 

A symptomatic diarrhea will, as a rule, be accompanied by signs 
of pathological dentition at points in the jaws, at which teeth should 
be in process of eruption. 

Nervous Disturbances. — Disorders referable to the central 
nervous system are the most alarming, and are those indicating the 
higher grades of severity of irritation. 

The milder forms of these are faint muscular twitchings and 
evidences of slight cerebral disturbance. 

Either of these may be the result of poisons absorbed from the 






1 American* System of Dentistry. 2 Oral Pathology and Practice. 



74 DENTITION 

alimentary canal during the course of intestinal fermentation, but as 
cases of even convulsions have occurred without other cause than 
teething apparent, and been relieved by lancing alone, the possibility 
of direct connection between teething and central nervous disturbance 
must be admitted. 

A distressing symptom, not easy to elicit on account of the age of 
the patient, is headache. The child is sleepless, and cries without 
apparent cause; it becomes quiet, partially from exhaustion, and 
after a period again commences sobbing. • The indication of central 
disturbance may at times be noted in the contracted pupils of the 
eyes and in throbbing arteries. The usual treatment, the adminis- 
tration of chloral hydrate and potassium bromide, with cold appli- 
cations to the head, furnishes relief which is frequently not complete 
without attention to the dental organs. 

In the more severe and dangerous cases, the evidences of disorder 
of the central nervous system become unmistakable. These appear 
as clonic convulsions or symptomatic eclampsia. While it is probable 
in many cases that reflex irritation from the process of dentition in 
itself is but a secondary cause of convulsions, yet evidence is sufficient 
to warrant its being regarded as a determining factor. In very many 
cases teething convulsions appear to indicate a neurotic family taint, 
and eclampsia may attend many disorders in children of this type, 
notably the mechanical and chemical irritation induced by the 
presence of large masses of indigestible food in the intestines. It 
would therefore seem a result of reflex action, the source of periph- 
eral irritation not being of prime importance. 

So-called teething convulsions occur usually at a time when several 
teeth are in process of eruption. The onset of the convulsion is 
rarely, although apparently often, sudden. If the child be closely 
observed, it is noted that a period of cerebral disturbance — fretful 
crying, evidences of headache, sleeplessness, etc. — is followed by a 
period of dulness and' somnolence, or the child may lie with eyes 
half open. Twitching of one or more groups of muscles may be 
observed; the orbicularis oris and other muscles of the lips, and the 
muscles of the eye, notably the superior and internal recti, may 
contract spasmodically. A common muscular spasm ushering in con- 
vulsions, is that of the abductor muscles of the thumb; the thumbs 
are drawn toward the palms of the hands. The abductor muscles of 
the feet contracting, the feet are drawn inward. This period may 
be ushered in by a sharp cry, the eyes roll upward with the lids 
half open, and consciousness is lost. The symptoms may disappear, 
the child awakening dazed and fretful; or it may sink into sleep. 
Unless the source of irritation be removed, or active therapeutic 



PATHOLOGICAL FIRST DENTITION 75 

measures be instituted, the eclampsia may return and in severe 
cases be the precursor of death. 

Infantile paralysis of a group of muscles, or even a single muscle, 
has been recorded, lasting from a few days to months, appearing with 
dentition and disappearing after it. In some cases it persists for 
life. 1 Strabismus (sixth nerve), if produced, may also persist. 

Skin Disorders. — It is so common as to be almost termed the rule, 
to find that when there are intestinal symptoms there are eruptions 
observable on the skin. The mildest form of these is an herpetic 
eruption about the mouth; in other cases papular and vesicular 
eruptions are observed upon the skin of the body and limbs. 

Occurring within the mouth, infection may be added and ulcerative 
stomatitis may occur upon the gums, tongue, lips, or inside of the 
cheek. 

Pulmonary Symptoms. — Pulmonary irritation may be expressed in 
laryngeal cough attending the eruption of teeth, and disappearing 
thereafter. 

Treatment of Pathological First Dentition. — This may be divided into 
prophylactic and remedial. The prophylactic measures include care 
as to pasteurization of milk or modified milk diet, sterilization of 
bottles, bottle nipples and rings, the prevention of the introduction of 
unclean fingers into the mouth of the child, and the antiseptic care 
of its mouth by frequent washings with a saturated solution of boric 
acid in water. This last may be applied to the mouth on a soft, linen 
rag wrapped on the forefinger. These measures, together with the 
proper feeding, ventilation, and care as to clothing, which should 
give comfort and not be in any way irritating, tend to prevent intes- 
tinal fermentation and to reduce the general irritability of the infant. 

Remedial Measures. — To reduce local hyperemia of the gum 
above an erupting tooth, a common domestic measure is valuable, viz., 
a small block of ice is placed in a corner of a clean napkin, and con- 
fined in place by a thread; the infant places it in its mouth at pleasure 
if old enough, or the nurse permits the child to bite upon it. The 
mechanical effect of biting upon a hard substance has added to it a 
degree of cold which lessens the local vascular engorgement. 

Any severe local irritation about erupting teeth should be relieved 
by thorough lancing of the gum. It is irrational that the child should 
be permitted to suffer from local irritation which may develop into 
more serious complications. 

This operation is performed by dividing the gum lineally over the 
incisors and cuspids before eruption, crucially over the cuspids after 

1 White, American System of Dentistry. 



76 DENTITION 

eruption of the cusps only, crucially over the upper first molar, and 
with an X-incisor over the upper second and lower first and second 
molars (Fig. 36). 

For severe cases Flagg advised the removal of a block of gum 
from over a molar. A cut is made parallel with the lingual side of 
the crown, a second parallel with the buccal side, a third parallel 
with the mesial side. A tenaculum is thrust into the block of gum, 
which is drawn tense, and then divided at the distal portion, prefer- 
ably with a pair of curved gum scissors. Lacking these latter, the 
bistoury may be used. 

The cut over the upper incisors should, if possible, be made a 
little to the outside of the cutting edge, that for the lower to the 
inside, in order that their crowns may take a proper direction toward 
occlusion. 

The instrument to be used is a sharp-pointed bistoury, as it 
penetrates well and permits a free draw cut. It is to be wrapped 
with tape or a strip of linen cloth until only one-quarter of an inch of 
the point is exposed. This precaution prevents accidental wounds. 
The child must be securely held by an assistant, the least sympathetic 
available. 

Flagg's method was to place the child upon its back across the 
lap of the assistant, w r ho, in one position, places his left hand over the 
child's eyes, securing the head; his right hand secures the hands upon 
the abdomen, while the legs are held against his body by the right 
arm. The position may be exactly reversed. The feet should be 
placed toward the light for the upper jaw, the reverse for the lower 
jaw. In another position the child sits upon one thigh of the assist- 
ant, the back of the head resting upon the chest, and the hand of that 
side (usually the right) pressed over the child's eyes to hold the head 
firmly. The other hand and forearm hold the child's hands and legs 
firmly. 

The operator encloses the gum about the part to be cut with the 
thumb and forefinger of the left hand, so that the bistoury cannot 
slip and cut lip, cheek, or tongue. Incision over the erupting tooth 
should be made until the knife-blade is felt to touch the enamel 
surface. The operation of scarifying the gums, making merely a few 
scratches to relieve engorged vessels, is but temporizing with the 
condition; the cut should be of sufficient extent to entirely remove 
tension from above the tooth. The little finger of the right hand may 
rest upon the chin of the child as an additional guard. 

If the child bite, a cork with a string attached for safety may be 
used as a prop. Asepsis, as in other oral surgery, should be observed. 

More or less bleeeding follows upon the operation, and, as a rule, 



PATHOLOGICAL FIRST DENTITION 77 

ceases spontaneously. A short period of bleeding is desirable, so that 
vascular engorgement may be reduced. Suckling by the breast or 
bottle usually serves to check the bleeding by compressing the tissues. 
In the event of the bleeding continuing, the mouth should be carefully 
examined, and a piece of ice in a napkin may be given to the child 
to suck. The child may swallow the blood and later regurgitate it. 
Obstinate bleeding may require the use of styptics, but these should 
be of a character to cause only coagulation of the blood, not the 
destruction of tissue. A little powdered tannin laid upon the cuts 
acts promptly, as does also a small amount of powdered alum. In 
some cases the internal treatment may be necessary. (See Hemo- 
philia.) 

Death has occurred from hemorrhage due to lancing, in cases of 
presumably hemorrhagic diathesis; so that inquiry as to family 
history would be a wise precaution. Obtaining such a history, the 
gravity of the symptoms alone warrant the operation. In the absence 
of such a history the operation is to be held as trivial. If it occur, it 
should be treated as indicated. (See Hemophilia.) 

The operation of lancing is warranted, even when the gum may 
be likely to heal over the tooth by formation of cicatricial tissue, 
provided symptoms demand it. It is contra-indicated in diphtheria 
and erysipelas, owing to the danger of infection. 

Shock has occurred in long-continued debilitated cases, and if 
feared, a trifle of brandy in water may be given previous to the 
operation. 

It is within the knowledge of the writer, that a physician has 
refused to lance the gums in a case diagnosed as cerebral menin- 
gitis, even when death was prognosed and though the child was at 
an age rendering pathological dentition possible, and in spite of a 
history of pathological dentition in a previous child at the same age. 
J. Lewis Smith 1 concedes the similarity of occasional symptoms of 
pathological dentition and cerebral meningitis, so that the above 
therapy was foolish, to say the least, and especially so in view of the 
probable death, which did occur. As a contrary specimen of judg- 
ment, a mother having a child with repeated convulsions "rubbed" 
the gums with a thimble until she "felt" the teeth, when the child 
sank into a peaceful sleep and had no more convulsions. In many 
desperate cases, lancing has effected marvellously rapid recoveries, 
aided by judicious handling of the accessory symptoms, even though 
all hope from ordinary therapy had been abandoned. Physicians in 
general refuse to lance, upon the ground that cicatricial tissue will 

1 Diseases of Children. 



78 DENTITION 

form and render the process of dentition more difficult. This is 
merely substituting a supposititious effect for a needed therapy. 
Observation renders it a question as to the knowledge of physicians 
of the location of the teeth and the pathological process of dentition. 
Even granting cicatricial tissue to possibly retard dentition, there is 
no difficulty in again lancing if conditions require it. 

Treatment of Stomatitis. — Should general stomatitis, with or 
without stomatitis ulcerosa, make its appearance, the mouth is to be 
promptly and freely sprayed with a 3 per- cent, solution of hydrogen 
sdioxid, followed by a spray of potassic chlorate (gr. xx to §j), which 
usually affords prompt relief. Should the spots of ulceration not 
disappear promptly, the mouth and tissues about the ulcer are to 
be guarded by soft linen napkins; each ulcer is dried and touched 
with carbolic acid, full strength. The spraying is to be repeated 
at intervals of three hours during the waking period. 

Treatment of Skin Eruptions. — The eruptions which appear 
upon the skin during dentition may be a source of annoyance to 
the child by causing itching. As a rule, measures directed toward 
a regulation of the intestinal functions cause a disappearance of the 
skin affections. If the eruption be widespread and cause much 
itching, a wash of phenol-sodique, diluted to one-third with water, 
usually affords relief. If the surfaces be then dried and talcum 
powder dusted over them the condition is much alleviated. About 
the mouth and over excoriated surfaces a zinc oxid ointment is useful. 

Treatment of Intestinal Symptoms. — The fermentative material 
in the bowel, together with the great mass of bacteria present, should 
be removed by the use of a cathartic. It is indicated in both con- 
stipation and diarrhea. Castor oil serves well, and is readily taken 
by children. To lessen the irritation of the bowel, laudanum and 
powdered acacia may be added. 

The following formula may safely be used even at six months of 
age: 

1$ — Tincturse opii gtt. x 

Olei ricini f5iss 

Pulveris acacise 5ij 

Saccharini gr. ij 

Aquae cinnamomi q. s. ad fgiij — M. 

Sig. — Shake the bottle, and give one teaspoonful each two hours if needed. 

For an additional six months of age, ten drops more of laudanum 
may be added to the general formula. In mild cases, olive oil in half- 
teaspoonful doses may be substituted. 

Following catharsis, antacid sedative astringents and intestinal 
antiseptics are indicated: 



PATHOLOGICAL FIRST DENTITION 79 

3 — Saloli 5J 

Bismuthi subnitratis 5ij 

Misturse cretse ad f5iij — M. 

Sig. — One teaspoonful every four hours. (Biddle.) 

1$ — Tincturae opii gtt. xvj 

Bismuthi subnitratis 5ij 

Misturse cretse f3iss 

Syr. simp f5iss — M. 

Sig. — Shake well, and give in teaspoonful doses every four hours. (Barrett.) 

The virtues of both formulae may be obtained by including the 
laudanum (gtt. xii) with the salol formula. 

Listerine in 10-drop doses, in water, every three hours, serves 
as an intestinal antiseptic. 

The gums are, of course, to be lanced at the outset, if the diarrhea 
be due to pathological dentition. Following the intestinal antisepsis, 
the general debility and possible intestinal toxemia are to have care- 
ful attention, and the child's food is to be properly adjusted to 
its needs. If the child is being nursed by a capable and healthy 
mother, this is to be regarded as the best form of food supply, but if 
not so nursed, proper artificial feeding is to be resorted to. 

J. Lewis Smith claims that upon the following diet, ill-conditioned 
children under his care in the hospital escape summer diarrhea and 
thrive; the diet is therefore here introduced. 

For children not nourished on breast milk of good quality, and 
those over three months, he recommends the following substitutes: 

1. Heat barley flour in a double boiler, the water in the outer vessel 
to be kept boiling for five to seven days, to burst the starch granules 
(Robinson's prepared barley flour can be bought). 

2. Take of this flour one tablespoonful, add 25 or 30 tablespoon- 
fuls of boiling water, and boil and mix for five minutes. Cool to 
blood heat, add 1 dram of diastase to change the starch to dextrin 
and maltose. Forbes' diastase or Taka-diastase can be bought. Of 
the latter, 1 grain will change 300 grains of starch to sugar, therefore 
a half-dram only need be used. 

Pasteurize milk by heating for twenty minutes to 160° F. Cool 
quickly on ice and let the cream separate. To two and one-half 
ounces of the upper half, add a little peptogenic milk powder (Fair- 
child's), to peptonize it. He mixes this peptonized milk with three 
and one- half ounces of the above dextrinized gruel at a meal, and feeds 
the infant nine or ten times, at two-hour intervals. Before feeding, 
he administers a few drops of a digestive ferment. 

For use in emergency, he recommends two heaped teaspoonfuls 
of condensed milk to fifteen teaspoonfuls of boiled water, as equiva- 
lent to seventeen teaspoonfuls of ordinary milk. 



so 



DENTITION 



He gives the following table of quantities of food required by 
infants; either breast or modified cow's milk to be used. 









Number of 


Total daily 


At each feeding. 






daily feedings. 


quantity. 


During the first week 


. 1 


ounce 


10 


10 ounces 


At the third week . 


14 


ounces 


10 


15 " 


At the sixth week . 


2 




8 


16 " 


At the third month 


3 




8 


24 " 


At the fourth month 


4 




7 


28 " 


At the sixth month . 


6 




6 


36 " 


At the tenth to twelfth month 


8 




5 


40 " 



White, following Starr, gives the following schedule of the diet of a 
hand-fed infant from birth upward, 1 which will serve as a suggestive 
and useful guide: 

Diet During the First Week. 

Cream f3iij 

Sugar of milk gr. xv 

Whey fgss, f5ij 

Water fgss, f5ij 

This portion to be given every two hours from 5 a.m. to 11 p.m., and in some instances 
once or twice during the night. 

Diet from the Second to the Fifth Week. 

Milk fgss 

Cream f3ij 

Sugar of milk gr. xv 

Water fgj 

This portion to be given every two hours from 5 a.m. to 11 p.m. 

Diet from the Fifth Week to the End of the Second Month. 

Milk f5J, f5ij 

Cream f§ss 

Sugar of milk gr. xxx 

Water . fgj, f3ij 

This portion to be given every two hours. 

Diet During the Third Month. 

Milk f§iiss 

Cream fgss 

Sugar of milk 5J 

Water fgj 

This portion to be given every two and one-half hours. 

Diet During the Fourth and Fifth Months. 

Milk fgiiiss 

Cream f§ss 

Sugar of milk 5J 

Water fgj 

This portion to be given every three hours. 



1 Diseases of the Digestive Organs in Infancy and Childhood, by Louis Starr, M.D. 



PATHOLOGICAL FIRST DENTITION 81 

Diet During the Sixth Month. 

Milk fgivss 

Cream fgss 

Sugar of milk 3J 

Water fgj 

This portion to be given four times daily. 

Two other meals — morning and mid-day — may be as follows: 

Milk fgivss 

Cream . fgss 

Mellin's Food 3j 

Hot water fgj 

Dissolve the Mellin's Food in the hot water, and add, with stirring, to the previously 
mixed milk and cream. 

In the seventh month, the Mellin's Food may be increased to two 
teaspoonfuls and given three times daily. 

Throughout the eighth and ninth months, five meals a day will be 
sufficient — at 7 and 10.30 a.m., 2, 6, and 10 p.m. 

Milk fgviss 

Cream f§ss 

Sugar of milk 3J 

Water . . f5j 

This portion for the first and last meals. 

For the other three meals, 1 tablespoonful of Mellin's Food may be 
added, or 1 teaspoonful of "flour-ball" may be given twice daily, 
instead of the Mellin's Food — say at the second and fourth meals. 

Diet for the Tenth and Eleventh Months. 

First meal, 7 a.m. : 

Milk f5viiiss 

Cream fgss 

Mellin's Food gss 

(Or "flour-ball" or barley jelly 3ij) 

Water fgj 

To be used only when Mellin's Food is employed. 

Second meal, 10.30 a.m. : Eight ounces of warm milk. 

Third meal, 2 p.m.: The yolk of an egg lightly boiled with stale 
bread crumbs. 

Fourth meal, 6 p.m. : Same as first. 

Fifth meal, 10 p.m. : Same as second. 

On alternate days the third meal may consist of 1 teacupful (f^vj) 
of beef tea containing a few stale bread crumbs. 

Beef tea, for an infant, is made in the following way : One-half pound 
of fresh rump steak, free from fat, is cut into small pieces, and put 
with 1 pint of cold water into a covered tin saucepan. This must 
6 






82 DENTITION 

stand by the side of the fire for four hours, then be allowed to simmer 
gently (never boil) for two hours, and, finally, be thoroughly skimmed 
to remove all grease. 

A further variation can be made by occasionally using mutton, 
chicken, or veal broths instead of beef tea. 

DIET FROM THE TWELFTH TO THE EIGHTEENTH MONTH 
(FIVE MEALS A day) 

First meal, 7 a.m.: A slice of stale bread broken and soaked in a 
breakfastcupful (f§ viij) of new milk. 

Second meal, 10 a.m.: A teacupful of milk (fgvj) with a soda 
biscuit or thin slice of buttered bread. 

Third meal, 2 p.m. : A teacupful of beef tea (f§ vj) with a slice of 
bread, 1 good tablespoonful of rice, and milk pudding. 

Fourth meal, 6 p.m. : Same as first. 

Fifth meal, 10 p.m.: One tablespoonful of Mellin's Food with 
1 breakfastcupful of milk. 

To alternate with this : 

First meal, 7 a.m. : The yolk of one egg slightly boiled, with bread 
crumbs; 1 teacupful of new milk. 

Second meal, 10 a.m.: A teacupful of milk with a thin slice of 
buttered bread. 

Third meal, 2 p.m.: A mashed boiled potato, moistened with 4 
tablespoonfuls of beef tea; 2 good tablespoonfuls of junket. 

Fourth meal, 6 p.m.: A breakfastcupful of new milk with a slice 
of bread, broken up and soaked in it. 

Fifth meal, 10 p.m. : Same as second. 

The fifth meal is often unnecessary, and sleep should not be dis- 
turbed for it. At the same time, should the child awake an hour or 
more before the first meal time, he should break his fast upon a cup 
of warm milk, and not be allowed to go hungry until the set breakfast 
hour. 

DIET FROM EIGHTEEN MONTHS TO THE END OF TWO AND ONE- 
HALF YEARS (FOUR MEALS A DAY) 

First meal, 7 a.m.: A breakfastcupful of new milk; the yolk of 
one egg lightly boiled; two thin slices of bread and butter. 

Second meal, 11 a.m.: A teacupful of milk with soda biscuit. 

Third meal, 2 p.m.: A breakfastcupful of beef tea, mutton or 
chicken broth, a thin slice of stale bread, a saucer of rice, and milk 
pudding. 



PATHOLOGICAL FIRST DENTITION 83 

Fourth meal, 6.30 p.m.: A breakfastcupful of milk with bread 
and butter. 

On alternate days: 

First meal, 7 a.m. : Two tablespoonfuls of thoroughly cooked oat- 
meal or wheaten grits, with sugar and cream; 1 teacupful of new 
milk. 

Second meal, 11 a.m. : A teacupful of milk with a slice of bread and 
butter. 

Third meal, 2 p.m.: One tablespoonful of underdone mutton, 
pounded to a paste; bread and butter, or a mashed potato moistened 
with good plain dish gravy; a saucer of junket. 

Fourth meal, 6.30 p.m. : A breakfastcupful of milk, a slice of soft 
milk toast, or a slice or two of bread and butter. 

The foregoing schedule must, of course, be regarded as an average. 
Many children can bear nothing but milk food up to the age of two 
or even three years, and provided enough be taken, no fear for their 
nutrition need be entertained. The rule to adopt is, if a child be 
thriving on milk, it is never to be forced to take additional food, 
merely because a certain age has been reached. Let the healthy 
appetite be the guide. 

The following is recommended by Starr as a modified milk diet, 

and as a substitute for mother's milk while weaning: 

» 

Pasteurized cream f 5 ss 

Pasteurized milk fgiiss 

Sugar of milk 3ss 

Water, boiled fgj 

Should this not satisfy the infant, increase the ingredients (except cream) to 6, 8, 
or 12 ounces. 

Hare 1 recommends the following diet list, followed in his hospital 
practice: 

DIET FOR A CHILD AGED TWO YEARS. 

Breakfast, 7.30 a.m.: Milk. The lightly boiled yolk of an egg; 
thin bread and butter (the bread to be one day old). 

Lunch, 1 1 a.m. : Milk. A thin slice of bread and butter. 

Dinner, 1.30 p.m.: Beef tea, or small piece of minced roast beef 
or mutton, devoid of gristle. One well-mashed potato, moistened with 
gravy. Rice and milk. 

Supper, 6 p.m. : Milk. Bread and butter. 

For drink: Boiled or filtered water. 

1 Practical Therapeutics. 






84 DENTITION 

DIET FOR A CHILD AGED ONE YEAR (FIVE MEALS A DAY). 

First meal, 7 a.m.: 2 teaspoonfuls of grated flour-ball (prepared 
as directed below) in § pint of milk. 

Second meal, 10.30 a.m.: J pint of milk with 4 tablespoonfuls 
of lime water. 

Third meal, 2 p.m. : The yolk of one egg, beaten up in 1 teacupful 
of milk. 

Fourth meal, 5.30 p.m. : Same as the first. 

Fifth meal, 11 p.m.: Same as the second. 

Flour-ball is to be made by taking one pound of good flour — 
unbolted, if possible — tie it up very tightly in a pudding-bag; put it 
in a pot of boiling water early in the morning, and let it boil until 
bedtime, then take it out and let it dry. In the morning, peel off the 
surface and throw away the thin rind of dough, and with a grater, 
grate down the hard, dry mass into a powder. To use this, take 
from 1 to 2 teaspoonfuls of the powder, rub it down until smooth 
with a tablespoonful of cold milk, and add 1 tumblerful of hot milk, 
stirring it well all the time. 

DIET FOR A CHILD AGED FROM SIX TO TWELVE MONTHS (FIVE 
MEALS A DAY). 

First meal, 7 a.m.: Mellin's Food, 1 tablespoonful; or flour-ball 
grated, 1 or 2 teaspoonfuls (prepared as directed above) ; hot water, 
4 tablespoonfuls; warm milk, enough to make § pint. Dissolve the 
Mellin's Food, or rub down the grated flour-ball in the hot water by 
stirring, then add the milk; mix thoroughly. 

Second meal, 10.30 a.m., and third meal, 2 p.m.: A breakfast- 
cupful of milk, with 4 tablespoonfuls of lime water. 

Fourth meal, 5.30 p.m. : Same as first. 

Fifth meal, 10.30 p.m. : Same as second. 

Treatment of Nervous Conditions. — If nervous reflexes, great 
irritability, or cerebral congestion appear, attention should be 
directed to the condition of the bowels and the teeth. 

If constipation or diarrhea exist, a cathartic is given and the gums 
are lanced. A cerebral sedative is to be prescribed. 

T$ — Chloralis hydratis gr. ij 

Sodii bromidi gr. v 

Aquae menthae piperitae f3ij — M. 

Sig. — Per orem. One dose; enlarge formula for repetition as needed. 

If convulsions be threatened, the clothing should be loosened and 
cool applications made to the head. 



CONSTITUTIONAL STATES MODIFYING DENTITION 85 

If the child be in convulsions, it should be immersed to the waist 
in water as hot as can be borne, to which has been added 2 table- 
spoonfuls of common mustard flour, and cool water poured over its 
head, when, as a rule, the symptoms promptly subside. Chloroform, 
which children endure well, may be administered. 

After immersion, a rectal injection of 1 dram of glycerin or a 
glycerin suppository will usually cause a free stool. A cerebral 
sedative should be administered. 

1$ — Chloralis hydratis gr. ij 

Sodii bromidi gr. v 

Starch paste 5ij — M. 

Sig. — To be administered per rectum. (Atkinson.) 

« ■ 

It is well also to administer a cathartic, to unload the intestines of 
irritating substances possibly present. 

After sleep, if appearances indicating dental irritation be observed, 
gum lancing is practised. It is wise that this operation be thus 
deferred, as convulsions may be precipitated by the act of lancing 
when the nervous system of the child is overexcited. The removal of 
intestinal irritants, by a cathartic given per orem is also in order, 
before lancing. 

It has been repeatedly noted that when evidence of marked 
cerebrospinal irritation is present, for which no probable source can 
be assigned, and an examination of the gums shows no apparent local 
disturbance, yet if it be at a period when one or more teeth are in 
process of eruption, but are still covered or bound down by gum 
tissue, if gum lancing be practised, relief is immediate and the lancing 
may even avert a threatened attack of eclampsia. It is presumed that 
these are cases of pulp irritation, in which a failure of resorption of 
tissue in advance of the tooth crown has caused pressure upon the 
pulp forming the root end. 

CONSTITUTIONAL STATES MODIFYING DENTITION. 

Children who are the victims of hereditary syphilis, usually cut 
their teeth very early; the alveolar process being in many cases 
insufficient. Cases are recorded where children have been born with 
crowns of teeth visible upon the gum, there being no evidence of root 
formation, the crowns being loosely held to the gum by fibrous 
tissue. It is necessary to remove these loose crowns, to permit the 
infant to suckle. The presence of loose crowns of teeth is a condition 
pointing to, though by no means diagnostic of, hereditary syphilis. 
Particularly in children in whom a history of hereditary syphilis is 
obtainable, the process of dentition may be accompanied by rapid 



86 DENTITION 

and frequently widespread breaking down of the soft tissues, over 
and about erupting teeth. Local measures of treatment seem to be 
of but little avail, except that antiseptic treatment undoubtedly 
prevents complications from extraneous infection. In rachitis the 
teeth are generally delayed in eruption. A delay beyond the age of 
nine months while not evidence of rickets in itself should prompt 
suspicion of the disease and its prodroma should be looked for as 
described by J. Lewis Smith, M.D. It is a disease largely due to 
improper diet and bone starvation causing increased cell growth and 
imperfect deposition of lime salts so that the bones contain about 
20 per cent, of inorganic as against the normal of 67 per cent. 

There are said to be many cases of slight rachitis even among the 
well to do, though largely found among the poor and ill-nourished. 
The shape of the cranium is often altered, due to the brain and pillow 
pressure upon the soft bones. These craniotabes occur under one 
year, often under eight months of age. The other prodromal symp- 
toms are "indigestion, or intestinal catarrh with flatulence, unhealthy 
stools and poor and capricious appetite." 

Fretfulness, disturbed sleep, free perspiration from the head and 
neck with dry trunk and extremities, tenderness over a considerable 
part of the body due to the rachitic effect upon bones and muscles 
are other symptoms. Later skeletal changes occur resulting in 
deformities. Spasm of the glottis is due to the craniotabes. The 
treatment of the condition is purely medical. 

In children classified indefinitely as strumous, which may mean the 
children of syphilitic or tuberculous parents, or those with no such 
history whose surroundings are of the most unhygienic kind, the 
process of dentition may not only have an untoward course, but 
phagedenic ulcerations may occur. It is usually in the degree of a 
child's debility, either inherited or acquired through improper care, 
that dentition assumes morbid features. The treatment of such cases 
must be directed to raising the health standard. As local therapeusis, 
no measures seem more effective than the sprays of hydrogen dioxid 
first; next, potassium chlorate, and, if conditions indicate it, sprays of 
dilute listerine, which is stimulant, antiseptic, and slightly astringent. 

Infantile Scurvy. — Cases are reported in which the improper 
feeding of children has been followed by evidences of scorbutus. It 
occurs usually in bottle-fed babies confined to patent foods, the 
nutritive element being lacking. The gums become tumid, and 
hemorrhagic extravasations occur in their substance; the periosteum 
is stripped from the margins of the alveolar walls, the soft tissues 
hanging in discolored, pendulous masses about and beyond the teeth 
if any be erupted. 



THE SECOND DENTITION . 87 

The child is peevish, listless, and feeble. There is apparent pain 
in the limbs. 1 The urine may be bloody even, as a first sign. 

The treatment is largely systemic, and consists of using fresh cow's 
milk modified to conform to human milk, and in the administration 
of fresh lemon juice, preferably boiled, allowed to settle, and the 
supernatant fluid used, 2 or orange juice is also used. 

The mouth should be sprayed with sedative antiseptics, such as 
potassium chlorate in hydrogen dioxid. 

THE SECOND DENTITION. 

The permanent teeth are nearly all formed from cords given off 
at the sixteenth week from the sides of the cord of the corresponding 
temporary teeth as far back as the bicuspids, which are given off 
from the cords of the first and second temporary molars; the sacs 
are formed and lie lingual to and above the sacs of the temporary 
teeth (Figs. 41 and 42). At the fifteenth week of fetal life the 
cords of the first permanent molars are given off from the mucous 
membrane, at the third month after birth the cord for the second 
molar is given off from that of the first molar, and at three years 
after birth the cord of the third molar arises from that of the second 
molar. At birth therefore 44 teeth are in process of development and 
without doubt an impress is made upon the enamel organs by the con- 
dition of the mother. The same is no doubt true of all delicate tissues. 
As a prophylactic of the health or vital resistance of the child as well 
as for its good development of enamel the mother should have all 
possible dietary and hygienic consideration. After eruption and root 
completion in the temporary teeth and some development of the crowns 
of the permanent teeth the relation of the crypts of the permanent 
teeth to the temporary teeth is as shown in Fig. 40. 

By reference to Fig. 40, it will be seen that at six and one-half years 
of age, the twenty temporary teeth are still all in position, and that 
taking their places in the line of the arch, are the four permanent first 
molars, the roots of which are still incomplete. 

These molars do not replace any temporary teeth, but erupt back 
of the second temporary molars and during the "change" support 
the jaws with the assistance of the temporary molars until the per- 
manent incisors are fully erupted, and with the aid of the incisors, 
until the bicuspids come into occlusion. Their office as jaw props 
and organs of mastication during the change is, therefore, very 
important. Of their later function, more will be said farther on. 

1 Hare, Practical Therapeutics. 2 Ibid. 



88 



DENTITION 



At six and one-half years, the crowns of the permanent incisors 
lie in the relations shown, with the temporary central roots resorbed 
and the lateral root partly so. Their crowns are practically complete, 
but the roots are unformed. 

The cuspid crown in its crypt, lies well above and lingual to the 
unresorbed temporary cuspid root. The roots of the first and second 
temporary molars, a trifle resorbed upon the inner side, embrace the 
formed crowns of the first and second bicuspids. 

Fig. 41 



4 ^^^ 


^^-^ 




^""--•- ML ^ / 




*r #^ 




V9 • 




w ^ *rwji^ 



Tooth follicles for deciduous and permanent teeth, three months after birth: 1, 2, 
tooth sacs of deciduous teeth; 3, periosteum of hard palate; 4, tooth sacs of permanent 
teeth. (Broomell.) 

Fig. 42 




Deciduous molars with tooth sacs for permanent bicuspids attached to the gingival 

tissue. (Broomell.) 



In their crypts back of the first molars, lie the forming crowns of 
the second permanent molars. The third molars are not in evidence 
in the illustration, but their development is in progress. 

It will be seen that the permanent central and lateral incisors 
replace the temporary central and lateral incisors, the permanent 
cuspid the temporary cuspid, and the first and second bicuspids the 
first and second temporary molars, respectively. 



THE SECOND DENTITION 89 

From this age to adult age, as previously, the jaw undergoes constant 
change, enlarges by constant resorptions and depositions of bone, and 
changes its contour to conform to the changes occurring throughout 
the body, and to accommodate the permanent teeth, which are in 
general terms larger and more numerous than the temporary teeth. 

It is regarded as normal that at about four to five years of age 
spaces shall appear between the anterior temporary teeth due to the 
gradual enlargement of the arches due to developmental forces 
probably exerted in part by the descent of the permanent teeth, 
though development to a type or a vital element is also in action. 

It may be said that the alveolar process built about the roots of 
temporary teeth and the roots of the temporary teeth are all resorbed 
during the replacement of the latter, and that when the crowns of 
the permanent teeth are fully erupted, new alveolar process is built 
up about their roots. Any subsequent change in the position of the 
permanent teeth is accompanied by an alteration in the alveolar pro- 
cess, and after extraction the latter is resorbed, but upon an implan- 
tation (which see) being done, new process will form. Its dependence 
upon the teeth is, therefore, evident. 

The following table gives the approximate ages for the eruption 
of the permanent teeth: 

First molars 5J to 7 years 

Central incisors 7 to 8 years 

Lateral incisors 8 to 9 years 

First bicuspids 10 to 11 years 

Second bicuspids 11 to 12 years 

Cuspids, the lower usually preceding by a year or more 12 to 14 years 

Second molars 12 to 15 years 

Third molars 16 to 20 years 

and indefinitely beyond 

The Process of Resorption of the Temporary Roots. — After com- 
pletion of formation, the roots of the temporary teeth remain in this 
state but a short time, as their successors are ready to advance to 
their places. 

Comparing the ages at which resorption begins with the ages at 
which it is complete (eruption of permanent teeth) (see Fig. 43), it 
will be noted that approximately three and one-half years are required 
in all cases for the removal of the temporary roots. Therefore, to 
determine the age at which absorption begins, deduct three and one- 
half years from the date of eruption of the corresponding permanent 
tooth. The degree of resorption at any age is shown in the table. 
The exact degree may be determined by radiography (Fig. 47). 

At the time the permanent tooth begins its advance, it lies in a 
bony crypt above and lingual to its predecessor, except in the case 






90 



DENTITION 



of the bicuspids, which lie between the roots of the temporary 
molars (Figs. 40, 41, and 42). 

Fig. 43 




Decalcification of the deciduous teeth. The numbers indicate years. (Peirce.) 



Fig. 44 



Fig. 45 





The structure of the absorbent organ, 
showing multinucleated or giant cells 
(odontoclasts). (Tomes.) 

Fig. 46 



4 L> 



Showing the relations of an erupt- 
ing permanent tooth to its deciduous 
predecessor. A, A, A, odontoclasts 
in absorbent organ. 



Imprisonment of second temporary 
molar; resorption of its roots, with 
absence of second bicuspid. (Skiagraph 
by Custer.) 



Each crypt has its own follicle wall enclosing a permanent tooth 
crown. 



THE SECOND DENTITION 91 

In the follicular wall overlying the crown, appear large multinu- 
cleated cells, the origin of which is unknown, but which by some are 
thought to be transformed osteoblasts, by others leukocytes (Figs. 
44 and 45). The latter is the probable explanation, as analogous 
cells are found about tissues or foreign bodies about to undergo 
resorption anywhere in the body. (See Resorption.) In the par- 
ticular situation under consideration they are called odontoclasts. 
The tissue between the root and crown has by Tomes been given 
the name of the "absorbent organ" (Figs. 44 A, and 45). These 
giant cells have a solvent or digestive function not understood, but 
which is competent to remove both the organic and inorganic matter 
of cementum and dentin, and evidences of action upon enamel in 
other situations are not wanting. (See Resorption of Enamel.) 
That the solvent is acid, is shown by the evidence of decalcification 
about the area of resorbed enamel of unerupted crowns of some 
permanent teeth. It is a curious fact that no evidence of decalci- 
fication of the permanent crown has been demonstrated to result 
from the proximity of the multinucleated cells in cases of physio- 
logical resorption of roots. One at first thought might connect opaque 
spots with this process, but the fact of a good enamel glaze, as a rule, 
together with the depth of the spot makes it a totally difficult picture 
from the grotto-like resorption or the roughened decalcification. In 
all probability the enamel is protected by the presence of Nasmyth's 
membrane, which is resistant to acids. These cells are probably 
invited by irritation due to pressure of the advancing permanent 
tooth crown, as the resorption is almost always found at the point of 
approximation of the crown with the root, or, in other words, at the 
pressure point (Fig. 47). 

Cases of resorption of temporary roots without the presence of a 
permanent crown are, however, noted and explained by Tomes 
upon the ground that resorption is a vital act independent of the 
pressure exerted (Fig. 46). As resorption of permanent roots, 
however, has often occurred from pressure of the crown of another 
tooth and occurs at the pressure point in physiological resorption, 
localized irritation, even in the absence of a permanent crown, must 
be credited with a large influence in the process. It is to be remem- 
bered also that in the absence of the pressure, resorption often does 
not occur, at least for twenty-five or more years — e. g., when laterals 
are absent and the permanent cuspids erupt to the side of the 
deciduous cuspids (Fig. 52). 

According to Tomes, redeposition of cementum occurs in pre- 
viously resorbed areas upon temporary roots; a fact corresponding 






92 



DENTITION 



with effects noted in permanent roots. (See Resorption of Perma- 
nent Roots.) 

Teeth frequently erupt lingually or labially to their corresponding 
temporary teeth, both remaining in the mouth. It is almost invari- 
ably the rule, upon extraction to find that an oblique resorption has 
occurred, as is shown in the right upper skiagraph in Fig. 47, and 
generally a decided hyperemia is seen in the pulp extending upward 
for perhaps a quarter of an inch. 



Fig. 47 



Fig. 48 





Phases of resorption of temporary roots. 
(Skiagraph by Price. 1 ) 



Diagram illustrating the 
relation of a resorbed tem- 
porary root and the perma- 
nent tooth, also the involve- 
ment of the pulp as a part 
of the resorbent organ. 
Resorption of the interior 
of crown of a temporary 
tooth. From actual case. 



Doskow 2 has shown by the prompt loss, by absorption, of a fairly 
firm deciduous cuspid, crowned to bring it up to level and so to 
usefulness, that such an operation is inadvisable because of an inher- 
ent tendency of an absorbent organ to become established. Again, 
a permanent tooth undergoing resorption often remains firm, until 
suddenly the strain becomes too great. 

As the root of the temporary tooth disappears, the pulp continu- 
ously fuses with the absorbent organ, so that when the crown alone 
remains, the pulp is still vital (Figs. 44 and 48). At times, it seems 
to take up the resorbent function and resorbs the crown dentin in 
some cases almost entirely. In one specimen, a circumscribed portion 
of the cementum and of enamel were removed by it, at the point of 
junction. This constituted practically a case of perforation by 



1 Items of Interest, 1901. 



3 Dental Cosmos, 1907. 



THE SECOND DENTITION 



93 



resorption (Fig. 48). The tooth was at first thought to be suffused 
with hemoglobin, as it was of a pink color. After extraction the 
absorbent organ was found as a papilla attached to the gum. At 
times, bay-like excavations in the crown dentin occur (Fig. 159, D). 
Dr. A. B. Harrower presented the writer with a radiograph of a 
case in which a second temporary molar retained at thirteen years 
excited doubt as to presence of a bicuspid successor. The bicuspid 
crown lay within the crown of the temporary molar, the dentin of 
the latter entirely resorbed (Fig. 49). When the root resorption 
reaches the point shown in the central incisor in Fig. 40 the tempo- 
rary tooth is loosened, moves about, and annoys the child, who may 
pick it out, or it is removed by extraction. 



Ftg. 49 




Bicuspid within the crown of a temporary molar. Note formative organs below root 
end. Practice of Dr. A. B. Harrower. 



Formation of the Roots of Permanent Teeth. — The extent of root 
development at any age is of great importance in view of canal thera- 
peutics. Incomplete roots present a mechanical difficulty of sealing 
the apex of the canal. The size of the pulp at the apical foramen 
of such teeth contraindicates the use of arsenic, and even pressure 
anesthesia is often unsuccessfully applied. 

The roots are developed in precisely the same manner as in the 
case of the temporary teeth, by the combined deposition of cementum 
by the osteogenetic cells of the follicle wall, which is drawn up on 
the root as a pericementum, and dentin by the odontoblasts of the 
papilla, which is drawn up as a pulp (Figs. 39 and 49). 

The extent of development of any of the permanent teeth may be 
seen at a glance by reference to the valuable table of Peirce (Fig. 50) . 
So graphically does this table give the desired information that 
explanation becomes unnecessary. It may here be noted that the 
end of a completed root is composed of cementum and that the apical 
foramen is not always single but may often be multiple or delta-like. 
(See Index.) 



94 



DENTITION 



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O 00 CO ■* 

<N ,-1 rH T-l 



c3 c3 c3 c3 OJ r 

o> o> a> cu £> £> 

>> >» >> >> £ £ 

<N O O CO iO S 



Irregularities of Second Dentition. — Some temporary teeth may 
be retained long after adult age is reached. The teeth most subject 
to this are the cuspids and second temporary molars. 

In the case of the cuspids, 
the permanent cuspid is de- 
layed or takes an unusual 
direction, erupting lingually 
or labially, or at times being 
directed into the place nor- 
mally occupied by the lateral 
incisors, which are wanting, 
or very rarely, the cuspid 
erupts posteriorly to the first 
bicuspid. At about forty 
years of age, the temporary 
cuspids may be lost by re- 
sorption of their roots, but 
until such time should be 
retained if usefully filling a 
space. If in interference 
with proper alignment or 
eruption of the permanent 
cuspid, they should be ex- 
tracted. Their late resorp- 
tion is somewhat pathological 
in character, and probably 
due to or incited by a partial 
resorption of the root end 
during the descent of the 
permanent cuspid (Figs. 51, 
52, and 53). 

The late enforced loss of 
the temporary cuspid indi- 
cates the advisability of an 
implantation operation, 
though a small bridge held 
by a Carmichael attachment 
to the first bicuspid and a 
lug against the lateral or cen- 
tral is very useful. 

The molars are retained, 
as a rule, because of an ab- 
sence of permanent crowns 




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00 b- CO iO "* C? £? j=* ^ 



THE SECOND DENTITION 



95 



to cause resorption, although this may occur without such pressure 
(Fig. 46). I have seen a case of an adult lady with eight deciduous 



Fig. 5 




Absence of upper left lateral incisor, with permanent cuspid in its place; two 
temporary cuspids retained. Man, aged twenty-five years. 

Fig. 52 




Absence of upper lateral incisors and right bicuspid. Retention of temporary cuspids. 

From an adult. 

molars in place. The question of the abnormal development or 
absence of permanent germs, or of the state of the roots of the 
temporary tooth may be settled by radiography (Figs. 47 and 54). 






96 



DENTITION 



The question of extraction or retention depends upon the diag- 
nosis. A firm temporary tooth should never be extracted simply to 
allow a permanent tooth to erupt unless the presence of a permanent 



Fig. 53 



E3 



Fig. 54 



Permanent cuspid erupted posterior to the first bicuspid. 

tooth in the jaw, as determined by radiograph or other means, gives 
reasonable inference that the permanent tooth is held back by the 
temporary tooth. In most cases a reasonable delay is advisable. 
A patient of the writer's wore a plate for thirteen years because of the 

injudicious extraction of an upper 
temporary cuspid, the permanent 
tooth appearing at twenty-six years 
of age. 

When the retention of temporary 
molars and cuspids occurs, they are 
apt to occupy an occlusal level, lower 
than that of the permanent teeth 
(Fig. 46). They may not be in 
occlusion at all, as was the case with 
the eight molars just referred to. 
This proves the fact that the general 
occlusal level of the permanent teeth 
is farther from the margin of the alveolar process than in the case of 
the temporary teeth. The length of the permanent crowns accounts 
for this. In normal replacement, however, the occlusal level is nearly 
the same for the temporary molars and first permanent molar, at 
least until the change is made by the eruption of the bicuspid. 

The devitilization of the pulp of the temporary tooth may delay 
resorption and indicate extraction. The imprisonment of a temporary 
molar has been accompanied by neurotic or mental symptoms 
supposedly cured by the extraction which is rational. It is to be 
remembered that in case of premature extraction of temporary 
teeth the date of eruption of the permanent successors is usually 




Retained temporary molar with bi- 
cuspid present. (Radiograph by E. 
Ballard Lodge.) 



THE SECOND DENTITION 



97 



earlier by a year or two, of which fact advantage may be taken 
especially in cases of devitalized temporary molars. 



Fig. 55 



Fig. 56 







Retained lower temporary molars, Delayed cuspid. (Radiograph by E. 

bicuspid absent. (Radiograph by E. Ballard Lodge.) 

Ballard Lodge.) 

Fig. 57 




Typical occlusion. (Cryer.) 



The correct placement of these first permanent molars seems to 
determine the correctness of molar occlusion, at least in the mesio- 
distal relation, though they may not occupy their correct bucco- 
lingual positions. Any slight forces disturbing the mesiodistal 

7 



98 DENTITION 

relation, causing the upper first molar to drift anterior to its correct 
occlusion with the lower molar, will result in an abnormal relation 
of the teeth to those anterior to them and to their antagonists; either 
upper protrusion or upper irregularities will occur. 

If the reverse occur, and the lower molar be placed anteriorly, and 
the upper be placed normally or posterior to its normal position, 
prognathism of the lower teeth ordinarily results. If placed too far 
posteriorly, retrusion of the lower teeth will occur. 

Fig. 58 




Malocclusion. Class I. (Angle.) 

According to Angle, the misplacement of the permanent teeth 
erupting early causes their inclined planes to direct other teeth from 
normal occlusion, or by permitting contraction of the space normally 
occupied, particularly in the lower jaw, permits the other teeth to 
assume a position in a contracted arch, thus again causing their 
inclined planes to cause contraction in the opposite arch, with a 
consequent displacement, buccolingually, of teeth which would other- 
wise normally align themselves in the arch. Once established, the 
cheek and lip pressure maintains the inharmony (Fig. 62). 

Angle divides all irregularities into three classes, with divisions 
and subdivisions: 



THE SECOND DENTITION 



99 



Class I. — The first molars are correctly occluded mesiodistally, 
the teeth anterior being in malocclusion, though the biscuspids may 
be in correct mesiodistal relation. 

The general characteristic of the class is that shown in Fig. 58. 

Class II. — The lower first molars occlude distally to the upper 
first molars, causing retrusion of the lower jaw. Division I is char- 
acterized by distal occlusion on both sides, the upper arch is narrowed, 
the upper incisors lengthened and protruded. The upper lip is short 
and functionless, while the lower lip is thickened and rests cushion- 





Fig. 


59 




468 


■ 


^m"' 


^^C^S 


^Hir^' 




^^H^Jv ' *^' ^M 


■L-. -.1 


468 


468 JjjjH 


■ ■'*< .TJH 




H' 1 


l^H ' l" > • ~z-2n ~3t^B^^| 




I^**tS^c^>? ^ 


I 'RIGHT f*^^H 




■^468 VS " LEFT 1 



Malocclusion. Class II. (Angle.) 



like between the upper and lower incisors, increasing the protrusion 
of the upper and the retrusion of the lower. There is usually mouth 
breathing, due to some form of nasal obstruction. 

Division I. — The characteristic exists on one side only, the other 
being normal. Mouth breathing is usually associated (Fig. 59). 

Division II. — There is distal occlusion on both sides, but the 
upper incisors are retruded instead of protruded, with crowding in 
the cuspid region. These are associated with normal breathing 
(Fig. 60). 



100 



DENTITION 



Subdivision, Division II. — The characteristic is upon one side 
only, normal breathers. 

Class III — Division I. — In this class, the lower first molars occlude 
mesially to the upper first molars on both sides, and the lower jaw 
progressively protrudes anteriorly (Fig. 61). 



Fio. GO 




Malocclusion. Class II. Division II. (Angle.) 



Subdivision, Class III. — The mesial occlusion is upon one side 
only, the other being normal, the arches crossing in the region of the 
incisors. 

Angle has formulated the law "that the best balance, the best 
harmony, the best proportions of the mouth in its relations to the 
other features require that there shall be the full complement of 
teeth, and that each tooth shall be made to occupy its normal 
occlusional relations. He also states that the best development of 



THE SECOND DENTITION 



101 



the bones of the face and throat, the size and function of its cavities 
are dependent upon the position of the teeth. 

Fig. 61 




Malocclusion. Class III. (Angle.) 



Fig. 62 



The specific causes inducing malocclusion of the teeth as classi- 
fied above are: 

1. Premature loss of deciduous teeth prevents the pressure of the 
first molars upon the teeth anterior to them, which mechanically aids 
in the development of the jaws and thus of the space necessary for 
accommodation of the permanent teeth. It 
also allows the first molar to drift forward and 
come into malocclusion, and also to close the 
space occupied by the deciduous tooth, thus 
lessening space for its successor and forcing it 
into buccal or lingual displacement. The same 
is true of loss of approximal tooth contact as 
the result of caries (Fig. 62). For this reason 
the prophylaxis_of orthodontia demands the 
retention of the space for normal eruption of the 
permanent teeth by fillings or mechanical devices 
if necessary. 1 

2. Prolonged retention of deciduous teeth may cause a deflection 
of the temporary successor or prevent its eruption. 

3. Through loss of permanent teeth on that side upon which the 
tooth is extracted, the development of the jaw will be prevented 




Effects of the prema- 
ture loss of a deciduous 
second molar. 



1 For the prophylaxis of malocclusion and sequelae, the reader is referred to articles 
by J. Lowe Young, Dental" Cosmos, October, 1815; E. A. Boyne, Dental Digest, 1916, 
and M. T. Watson, Dental Items of Interest, April, 1916. 



102 DENTITION 

and the tooth posterior to the space will tend to tip or drift forward 
into malocclusion. 

4. Tardy eruption of permanent teeth permits closure of the space 
altogether or in part, and the resistance offered causes a deflec- 
tion of the tardy tooth (Fig. 62). The total absence of certain 
permanent teeth may be placed under this heading. 

5. Supernumerary teeth, by occupying space, also compel the 
normal teeth to take an abnormal position, and, if erupting after 
them, may displace them by constant pressure (Figs. 171 and 210). 

Fig. 63 Fig. 64 





Case of adenoids. Fig. 63, before operation; Fig. 64, after operation. (Faught.) 

6. Habits such as thumb and lip sucking or lip biting will move the 
upper anterior teeth outward and the lower anterior teeth inward. 
Holding the tongue between the anterior teeth produces infra- 
occlusion of the anterior teeth, while the constantly open mouth per- 
mits supra-occlusion of the molars. 

7. Nasal obstructions occurring in the developing child produce 
mouth breathing, and the opening of the mouth causes contraction 
of the muscles upon the teeth and bones, producing abnormalities 
of the bone of the jaw; the irregularity of Class II (Division I), an 
undeveloped nose and adjacent region of the face. Faught has ably 
illustrated these conditions in Figs. 63 to 71. ! The consideration of 
malocclusion as a general subject is properly relegated to special 
works, and the reader is referred to Angle's Malocclusion of the Teeth 
and other works on the subject. 

1 Dental Cosmos, 1908, p. 7. 



The second dentition 



103 



Disorders of the Second Dentition. — The devitalization of the 
pulp of a temporary tooth and proper canal filling delays, but does not 



Fig. 65 



Fig. 66 





Diagrammatic sagittal section, show- 
ing relation of anatomical landmarks. 
(Faught.) 



Adenoid vegetations. Compare Fig. 
65. (Faught.) 



Fig. 67 




Diagrammatic coronal section through head in the region of the first molar, 
showing nasal septum, uncinate process, inferior meatus, inferior turbinates, middle 
ethmoidal cells, middle turbinates, and hiatus semilunaris. (Faught.) 



absolutely prevent, resorption. Chronic abscesses upon such roots 
destroy the absorbent organ, but some pathological resorption may 
occur, as in case of permanent roots (which see). Pus has an alkaline 



104 DENTITION 

reaction which may neutralize the acid solvent. As a rule, such roots 
are mechanical obstructions to the permanent crowns, which are 
deflected to one side and caused to erupt irregularly; again, the 

Fig. 68 




Hypertrophy of right inferior turbinal, also deflected septum and spur. 
Compare Fig. 67. (Faught.) 

temporary root may be bodily pushed aside, its apex pressed against 
the alveolar process and gum tissue, which are resorbed, and the 
necrotic root end is seen extruded through the gum. Extraction is 
indicated. 

Fig. 69 




Cystic middle turbinal, hypertrophied inferior turbinals, enlarged middle ethmoidal 
cells, and hypertrophied middle turbinal. Compare Fig. 67. (Faught.) 

When temporary roots are not thus mechanically removed they are 
gradually extruded and decayed, or suppurative processes cause the 
resorption of the alveolar process about them. 



THE SECOND DENTITION 



105 



Injudicious retention of temporary teeth may thus cause an irregu- 
larity. On the other hand, premature extraction by permitting the 
approximation of the previously erupted permanent teeth may have 
an equally bad effect upon an erupting tooth (Fig. 62). 

In anticipation of physiological resorption of temporary roots, all 
temporary teeth should be carefully watched, cleansed, filled, and, if 
necessary, their roots treated so that a normal replacement by the 
permanent teeth may occur. If pronounced disease occur just 
previous to the time for normal replacement, extraction is indicated. 

Early extraction has sometimes caused early eruption of the per- 
manent teeth, e. g., bicuspids at seven years of age. 



Fig. 70 



Fig. 71 





Hypertrophied posterior end of inferior 
turbinal. Compare Fig. 65. (Faught.) 



Nasal polypi. Compare Fig. 65. 
(Faught.) 



It will be recalled that the teeth are an evolution of the dermoid 
system, which fact possesses pathological significance in certain acute, 
specific skin diseases. It is noted in some cases of the eruptive 
fevers of children, particularly when the child is much debilitated, 
that after the cessation of the acute disease, a necrotic affection of 
the jaw occurs, involving the alveolar bone and its contents. As 
many of these cases occur between the ages of three and seven years, 
the temporary teeth are still in situ; these, with the partially devel- 
oped permanent teeth and the enclosing bone, may be exfoliated. 
The necrotic process may involve but one tooth, or may include 



106 



DENTITION 



all of the temporary teeth, their successors, and a large mass of 
bone. 1 The disease with which this necrosis is most frequently 
associated is scarlet fever; 2 it is also found as a sequel of measles 
and smallpox. "The cases prior to exfoliation of the bone, exhibit 
a stripping of the periosteum, apparently beginning about the necks 
of the teeth. A discharge of pus having a fetid odor is present, and 
the soft tissues may be raised from the bone for a variable extent;" 
that is, there is evidence of purulent periostitis. In the course of 
some weeks, six or eight, the necrotic bone and its contents exfoliate. 
Salter observes that the sequestra forming after severe scarlet fever 
are much more extensive than those which form as a sequel of measles. 
An interesting case of bilateral sequestra of the aveolar process 
due to typhoid fever alone is reported by Cowper. 3 Two sound 
teeth were involved in each sequestrum. (Fig. 72.) 



Fig. 72 




Right. Left. 

Labial aspect of bilateral sequestra apparently due to typhoid fever alone. (Cowper.) 



The administration to children, of mercurials, has caused such a 
loss of teeth and process. I have seen a sequestrum containing three 
undecayed teeth attributed to this cause, and others have been 
reported. In these cases the parts should be kept as aseptic as 
possible by means of hydrogen dioxid and the compound tincture 
of capsicum and myrrh (enough to cloud a glass of water), used as a 
stimulant mouth wash. 4 When loose, the sequestrum should be 
removed. The parts heal by granulation, if due attention be paid 
to the general physical welfare of the child. 

Eruption of the Molars. — The first permanent molars rarely 
produce more than slight rheumatic pains. The gum irritation 
may be relieved by an X-incision, or at times by the application 



Salter, Dental Pathology. 
Dental Cosmos, 1909, p. 765. 



2 Ibid. 

* Garretson, A System of Oral Surgery. 



THE SECOND DENTITION 107 

of phenol-sodique and laudanum, equal parts, or phenol camphor, 
with the finger tip. A little alcohol or dilute tincture of iodin serves 
almost equally well. 

As some time may elapse between eruption and occlusion, the first 
molars do not receive a proper friction. Associated frequently with 
carious temporary teeth, they are frequently decayed in their sulci 
and fissures; to prevent this it has been recommended that oxy- 
phosphate of zinc be placed over these fissures without previous 
excavation. 1 The oxyphosphate of zinc or copper may also be thus 
used in third molars which are even more liable to dental caries. 

The lower second molars may cause some irritation owing to an 
insufficient development of the jaw at the angle, leaving an inade- 
quate accommodation for the crown. At about nine years of age 
the second molar occupies the angle of the jaw in much the same 
position as shown in Fig. 73 for the third molar. If held back, a 
pathological condition equivalent to that oc- 
curring in the temporary teeth may result; FlG - 73 
reflexes producing heavy pains about the jaw 
or reflex effects, such as chorea, may be pro- 
duced. 

Truman 2 has prevented a threatened 
second attack of this sort by deep incisions 
in the gum over the site of the crown. The 
presumption is that such treatment relieves 
the tension upon the pulp underlying the ^" 

j i . Condition of third molar 

developing root. . at thirteen years of age . 

Kirk 3 calls attention to the liability of (Radiographed by Custer.) 

chorea to be associated with reflexes from the 

dental region at from four to nine years of age, and cites a case from 
the practice of C. N. Peirce in which choreic manifestations were 
permanently relieved by the removal of a deciduous molar inter- 
fering with the eruption of its permanent successor, the bicuspid. 
He also cites a case of repeated hysterical manifestations, following 
nervous irritability due to each replacement of a deciduous tooth by 
its successor. Flagg cured a case of chorea in a boy, by the extrac- 
tion of four teeth from a very crowded arch. 4 

The third molars frequently induce pathological conditions. 

The upper third molar, meeting in its descent the roots of the 
second molar, may be united to it by hypercementosis — the condition 
of concrescence (which see) ; escaping this, it may meet a dense palato- 
alveolar plate of bone at the tuberosity and be deflected buccally 

1 L. Ashley Faught. 2 International Dental Journal, 1899. 

3 Dental Cosmos, 1905. 4 Private communication. 




108 DENTITION 

through the thinner buccal plate of bone, so that its occlusal face 
presents cheekward (Fig. 74). Its occlusal face may present more 
posteriorly or more anteriorly. Here retained food collects about 
it and caries occurs, or a suppurative inflammation of the cheek 
or free gum margin may occur. For this condition sterilization, free 
incision of the gum margin, and subsequent asepsis maintained by 
antiseptic sprays will reduce the inflammation, which, however, is 
apt to recur at intervals. If the cheek be irritated or the position of 
the tooth permanently fixed, only traction of the tooth into a correct 
position, grinding away of the sharp cusps, or extraction will alle- 
viate the condition. The extraction of such a tooth is little loss to the 
individual. A bit of cotton saturated with a mild antiseptic may 
be placed between the tooth and cheek for a time after grinding. 
The possibility of concrescence in such a case, as shown in Fig. 74, 
must be considered when extraction is intended. Individual motion 

Fig. 74 Fig. 75 




Abnormal eruption of the upper third Partial eruption and impaction of third 

molar. molar. (Radiograph by Custer.) 

is diagnostic of separate teeth, and is readily induced, when the 
crowns are together, by pressing a strong, thin, flat-bladed instru- 
ment between the teeth and turning it. The teeth are seen to move 
apart. 

The pressure of an erupting third molar upon the second molar 
may cause neuralgic pains, and at times the teeth in general, as far 
forward as the central incisor, may seem to loosen up and become 
tender to touch and again become comfortable and tight. These 
symptoms may be repeated apparently in consonance with the efforts 
at eruption. This pressure also causes irregularities of alignment 
or breaks up an orthodontia. Their extraction for this reason is 
sometimes indicated. The third upper molar may be impacted with 
its face inclined toward the second molar root and may cause resorp- 
tion. (See Impaction.) 

Owing to insufficient development at the angle of the jaw, or 
density of the bony capsule due to chronic mild irritation from any 



THE SECOND DENTITION 109 

cause or some malposition of the tooth itself, lack of room due to a 
general malocclusion from any cause or perhaps to some malnutri- 
tional condition in the patient — singly or combined — it is almost the 
rule that the eruption of the lower third molar is attended with some 
degree of discomfort due to gum and bone irritation, and, possibly, 
to pressure on the formative pulp (Fig. 73). 

For some months prior to eruption, heavy, gnawing, rheumatic 
pains may be indefinitely located about the jaw and ear of the 
affected side. The muscles of mastication become stiff and may 
contract spasmodically, simulating trismus. These symptoms, if 
severe, may be relieved by deep X-incisions in the gum; or, if mild, 
by the application of non-discoloring rubefacients or sedatives to 
the outside of the face, over the affected parts. The massage of the 
parts affords some relief. Flagg recommended the following: 

1$ — Tinct. opii, 

Tinct. aconiti, 

Chloroformi p. aeq. — M. 

Sig. — To be rubbed on the outside of the face. 

Or, 

]$ — Aconitinae gr. ij 

Cerati simplicis 5J — M. 

Sig. — To be well spatulated. To be distended with oil of cloves or phenol 
camphor and gently rubbed on the outside of the face, the mouth and eyes to be 
particularly avoided. 

Or, when the aconitine fails to produce relief: 

]$ — Veratrinae gr. xx 

Cerati simplicis 5J — M. 

Sig. — To be used in the same manner as the aconitine. 

As the tooth advances, the symptoms may become progressively 
severe. The gum may become inflamed, swollen, and be masticated 
upon, the oral pyogenic organisms produce infection, presumably 
finding an entrance at the point proximating the second molar. The 
patient suffers from the pain and inability to masticate and swallow, 
and becomes nervous, irritable, and debilitated; the breath becomes 
fetid and the salivation excessive. The inflammation extends into 
the contiguous tissues, and pus may form, extending into them; 
swelling may occur in the adjacent glands, parotid, submaxillary, etc. 
It may also extend to the tonsil or pharynx. All mastication is pre- 
vented, fever is present, and the patient prostrated; septicemia and 
death may follow. 1 Reflex pains may occur. Neuralgia and even 
nervous and mental disturbances may occur (see page 72). Brown 2 
relates a case of noma which developed from an infection in this 

1 Flagg, and occasional reports, 2 Dental Cosmos, 1908, p. 5. 



110 DENTITION 

location. The gangrenous condition extended to the lungs. Death 
ensued. 

Brown also calls attention to cases of cancer diagnosed as patho- 
logical eruption. Perhaps private practice is more immune but I 
have never had such a development either privately or in clinical 
experience. 

Results similar to these may occur when the crown is partly 
erupted, being covered at its distal portion by a curtain of gum 
which may be ulcerated upon its under * surface. This curtain of 
gum may be thin and stretched, or project rather rigidly over the 
tooth without stretching, as though attached to it, sometimes a strap 
of gum crosses the tooth crown. 

In these latter cases the pus, as a rule, finds egress, but occasionally 
it burrows into the pocket between the tooth and contiguous tissue, 
causing much inflammation or pus formation which may invade the 
cheek muscles or involve the inferior dental canals. When gum 
pockets remain about teeth, food may ferment in them and cause 
deep pus formations which may result in Ludwig's angina, a frequently 
fatal disease. (See Ludwig's Angina.) 

In some case necrosis may ensue. Fortunately untoward experi- 
ence is rather rare, most cases responding to proper treatment. Other 
phases of pathological eruption of third molars will be considered 
under impactions. 

Treatment. — The treatment depends upon the stage to which the 
inflammation has advanced and the position of the tooth. 

In cases more particularly due to gum infection and inflammation 
rather than impaction, if the patient be able to partly open the 
mouth, the part may be sterilized by spraying it with a germicide 
such as a 1 to 2000 solution of mercuric chloride in hydrogen dioxid 
(or hot carbolized water, followed by application of tincture of iodin 
(Brown) or by injecting iodin trichlorid, 1 to 100). (See Index.) Fol- 
lowing this an injection of novocain solution is made into the flap 
of tissue, or a conductive anesthesia done and the gum completely 
removed from over the face of the crown, or, if feasible, any pocket 
wall cut away. 

To accomplish this, a deep linear cut is made with a sharp bistoury, 
extending from the distolingual to the mesolingual angle of the 
crown, if it need go that far. A similar cut is made from the disto- 
buccal to the mesobuccal angle. If not already free, the gum is 
divided at its mesial contact with the distal surface of the second 
molar. The block is now penetrated by a tenaculum, drawn tense, 
and the final cut made at the distal border with decidedly curved 
gum scissors. Less cutting is required in some cases. A special gum 



THE SECOND DENTITION 



111 



guillotine is obtainable, which practically bites out a piece of the 
gum flap (Fig. 76). Its use is limited to simple flaps. The electric 
cautery may be used to burn away the gum tissue. Even without 
anesthesia a white hot cautery is not very painful and eliminates 
bleeding. 



Fig. 76 




Ash's gum guillotine. 

The hydrogen dioxid spray should be again applied to remove any 
possible pus germs present, and should be repeated at intervals of 
about two hours; any pus pocket should be thoroughly flushed. Tinc- 
ture of iodin, diluted about one-half with alcohol, may be applied 
every few hours or much oftener by means of cotton wound on an 
applicator or tooth pick, arid exerts a germicidal effect. A 1 to 1000 



Fig. 77 




Gum scissors. 



iodin trichlorid wash for a time as recommended by Wass may be 
used (see Index). A neglect of antisepsis gave the editor a week of 
personal discomfort and inability to masticate, after the removal of 
a trifling and apparently non-inflamed flap of gum. A cold compress 
should be recommended for the angle of the jaw, if deemed advisable. 
Magnesium sulphate. as a derivative may be used with advantage. 
If the patient be confined to his bed and unable to open the jaws, 



112 DENTITION 

a more difficult operation presents. The first object should be to 
reduce the intensity of the inflammatory symptoms. This is accom- 
plished by the removal of the gum block as above, if the mouth can 
be opened sufficiently. Anesthesia may be resorted to, after oral 
sterilization, for the purpose. A jaw separator is introduced, and 
operated until sufficient space is gained and the cuts made. If no 
more be possible at the first visit, the lingual and buccal linear cuts 
should be made to insure free bloodletting, which may be increased 
by syringing forcibly with lukewarm water, the position of the 
patient being such that gravity favors its flowing out of the mouth. 

Cold compresses are to be placed over the angle of the jaw and 
magnesium sulphate and the hot pediluvium administered as deriva- 
tives. Cataplasma kaolini, a compound of kaolin (Chinese clay), 
boric acid, methyl salicylate, glycerin, and small quantities of thymol 
and oil of peppermint, 1 is useful, applied in quantity to the face, 
externally. The antiseptic sprays are to be used as before directed. 

If, in addition, local massage or the heat of a 100 candle lamp, and 
massage over the angle of the jaw be practised, the swelling and 
muscular hardness usually disappear in a few days. It is well to 
then remove the entire block of gum to prevent reinfection. There 
can be no question that complete anesthesia and thorough gum 
block removal, at the first visit, is the most advisable surgery. 

In case of suppuration deep in tissues iodin trichlorid as an injec- 
tion, 1 to 100, and, as a wash, 1 to 1000 (see Index) may be used and 
injections of a staphylococcus and streptococcus stock vaccine made 
hypodermically as suggested by Medalia. 2 (See Vaccine.) 

If the third molar be correctly placed, its eruption, as a rule, 
proceeds uninterruptedly from this point, though it may never be 
entirely free from some degree of overlapping by the gum tissue, 
owing to arrest of eruption by the occlusion of the more advanced 
upper third molar. Pockets are thus formed which favor food 
retention, which, undergoing fermentation, may either cause ulcera- 
tion of the soft parts, or caries of the distal and distobuccal surfaces 
of the tooth. If it be the cheek tissue that persistently overlaps, 
the tooth should be removed, but inflammation may temporarily 
be relieved by the above irrigation, and a pellet of cotton saturated 
with eugenol introduced for a short time. Grinding the occlusal 
face of the upper molar may assist eruption of the lower. 

More marked malposition may cause difficulty of eruption, 
necessitating the extraction of the third molar or even of the second 
molar in order to let it erupt or in order to reach it. In some cases 

1 Antiphlogistin is the proprietary equivalent. 

2 Dental Cosmos, January, 1914. 



THE SECOND DENTITION 113 

it may be better to also extract the upper third molar, as it will 
probably elongate in time and allow food to pack into the interspace 
mesial to it. A presentation of the occlusal face of the third molar 
to the distal surface of the second molar is a common form of mal- 
position. (Fig. 75.) 

The third molar may at times be diagnosed in this position by 
passing an explorer or thin right-angled blade down the distal sur- 
face of the second molar, or by means of a deep incision with a 
bistoury or exploring needle. Failing this, or preferably, replacing 
it, radiography is a very valuable means of diagnosis. Extraction 
of the third molar is indicated. 

Fig. 78 




The beaks of these forceps have been ground out so that they are similar to those 
of the "Kells" forceps. The bulge of the crown fits into the hollow beak so that the 
beak does not slip off. (Kells, Dental Cosmos.) 

Kells 1 cuts the occlusal half off partly with a small diamond or 
carborundum disk and saws the balance off with a dentate bur of 
extra length in the contra angle hand piece. The remainder of the 
crown is grasped with a right-angled Ash root forceps with beaks 
hollowed out. It is pulled forward. In all cases without special 
necessity for packing, irrigation with salt solution and the induction 
of a good clot is the best treatment. Extraction in such a case must 
be carefully done. The use of the elevator is dangerous, as there is 
danger of fracture of the ramus, which has occurred. (Schamberg.) 

In some cases a portion of the coronoid process should be removed 
to make a path for easy removal of the tooth. 

Deeply seated in this situation, pathological resorption of the root 
of the second molar may result, and irritation of its pulp be added 

1 Johnson's Text-book of Operative Dentistry. 

8 



114 DENTITION 

as a complication. In this case the second molar must be extracted 
and if not producing further ill results the third molar allowed to 
erupt as possibly useful. (See Malposition.) The alternative is 
the surgical removal of a portion of the coronoid process before 
removing the third molar. 

A more common form of presentation exhibits the distal surface 
of the crown above the gum and the meso-occlusal angle locked 
beneath the cervix of the second molar (Fig. 73). Caries is not in- 
frequently induced by the retention of food: The third molar may be 
removed by first cutting away the mesial obstructing portion and 
then lifting out with the forceps. 

Dr. George B. Winters is said to have demonstrated a successful 
technic for prompt removal of impacted lower third molars. I have 
solicited this but he prefers to delay publication to a later date. 

The operation is best done under conductive anesthesia. (Index.) 

In view of applied therapy it is well to remember that if a first 
molar be extracted before ten years of age the second molar will 
usually press forward into the place of the first and assume good 
alignment and occlusion. Likewise if the second molar be extracted 
early, the third will come into its place. The fact is valuable when 
decision must be made as to retention or extraction of diseased 
molars. Therefore after radiography to ascertain the presence of a 
worthy successor extraction at proper age may be advisable. 

The writer had a patient fifteen years of age with a badly decayed 
second molar with the pulp irritable. This was a good case for 
application of the principle, as the second molar roots were incom- 
plete at this age. 



CHAPTER IV. 
MALPOSITION AND IMPACTION OF TEETH. 

MALPOSITION OF TEETH. 

A tooth is malposed when out of its normal position and occlusion, 
though in some cases it may be in almost normal relation to its ad- 
joining teeth. 

The causes have been discussed in the chapter on Pathological 
Dentition, page 94. 

Fig. 79 




Case of seven lower bicuspids, two supernumeraries in place and one erupting. This 
patient has two supernumerary upper central incisors displacing the centrals proper, 
yet closely resembling them. Dr. Alfred Haas has shown me a similar model of a 
lower jaw with seven erupted bicuspids fiom which he already had extracted an eighth. 



Malpositions which are remediable through the application of 
mechanical force, applied by means of suitable apparatus, belong to 
operative dentistry. They are fully treated of in works upon opera- 
tive dentistry and orthodontia. 

The extraction of teeth after they have been erupted, or of their 
predecessors, is one of the most frequent causes of acquired mal- 
position of the remaining teeth. The teeth move from their original 

(115) 



116 



MALPOSITION AND IMPACTION OF TEETH 



Fig. 80 



positions, the anterior teeth, incisors, laterals, cuspids, and occa- 
sionally the bicuspids, having a tendency to drift posteriorly, some- 
times opening a space between the central in- 
cisors, sufficiently large to create a deformity. 
The molars have a decided natural tendency 
to drift forward, and when the bicuspids are 
removed they tip anteriorly, causing maloc- 
clusion upon their distal cusps and sometimes 
their distobuccal cusps alone, with a further 
tendency to tip forward and sometimes inward 
or outward .as well. Separation of the posterior 
teeth may occur, and in any event, the loss of 
mesial or distal support permits fibrous food to 
be packed between the teeth: as they spring 
slightly apart, it is held by their springing 
together again. The lack of occlusion brought 
about by extraction of antagonists permits 
elongation, and the loss of posterior support is apt to bring about 
labial protrusion or abrasion of upper anterior teeth. 

Fig. 81 illustrates a case of malposition of molar germs which have 
developed in the incisal region, displacing the incisors. 




Effects of premature 
loss of permanent first 
molars. 



Fig. 81 




Malposition of molar teeth. 

IMPACTED AND ENCYSTED TEETH. 

The extreme extent of dental malposition is reached when the per- 
manent teeth do not erupt at all. Instead of presenting in the dental 
arch, they may be entirely embedded in the substance of the bone, 



IMPACTED AND ENCYSTED TEETH 117 

either remaining there, with or without pathological manifestations, or 
erupting in some unusual situation. In other cases, a distinct cystic 
tumor forms about the enclosed tooth (Fig. 82). The cause of im- 
paction probably lies either in a previous malposition of other teeth 
preventing advance, or in an originally malposed tooth germ, or to 
the development of the root while the crown advance is retarded, the 
expulsive force of root formation being lost, or to bone condensation 
due to the stimulation from the effort at eruption or to other inflam- 
mation about adjoining teeth; to contracted arches due to mouth 
breathing or retarded jaw development and to acute infectious 
fevers causing inflammation of the bone. In many cases orthodontic 
procedures creating room may permit the descent of the tooth. 

Fig. 82 




Cyst of the lower jaw, having its origin about an undeveloped tooth. (Garretson.) 

Impacted Lower Third Molars. — By far the most common dental 
impaction is that of the lower third molar. The extent of impaction 
varies from a partial eruption, or partial imprisonment of the tooth by 
its bony surroundings, to its entire imprisonment in any part of the 
ramus. Many of the more severe cases treated under the head of 
pathological dentition, if unrelieved, would be included in the category 
of impacted teeth. 

Feldman 1 cites a case of impaction of a right lower third molar 
with unformed roots and associated with suppurative swelling, trismus 
and glandular enlargement. 

1 Dental Cosmos, 1918, p. 51. 



11$ 



MALPOSITION AND IMPACTION OF TEETH 



In Fig. S3 isshown a lower third molar presenting the effects of 
a previous impaction. The irritation caused by the efforts of the 



Fig. 83 




Right half of lower jaw, showing an impacted third molar. (Oyer.) 
Fig. 84 




Inner side of left half of same lower jaw. (Cryer.) 

tooth to disengage itself, or to overcome the resistance to its erup- 
tion, has caused an active formative reaction in the pericementum, 
resulting in a hypertrophy"of the cementum. Likewise the pressure 



IMPACTED AND ENCYSTED TEETH 



119 



upon the bone causes a condensing osteitis, and the bone becomes 
dense, more obstructive, and less vascular (see p. 49). 

If the distance between the posterior surface of the second molar 
and the columns of the coronoid process be very short, it is evident 



Fig. 85 




Impaction of lower third molar. Resorption of root of second molar and impingement 
of root upon inferior dental canal, which is deflected out of its course. (Cryer.) 

that upward eruption is impossible, so that the tooth may assume 
any direction of movement, the most common being forward, the 
axis of the tooth changing its position until the tooth may lie in a 
horizontal position or even become inverted. 



Fig. 86 



Fig. 87 





Impacted lower third molar beneath gum. 
Second molar tipped forward. (Radiograph 
by E. Ballard Lodge.) 



Impacted cuspid. (Radigraph by E. 
Ballard Lodge.) 



Fig. 84 is taken from the same jaw as Fig. 83, but shows the 
opposite side; the impaction is pronounced. Fig. 85 shows another 
case with different anatomical surroundings. In the first case there 



120 



[malposition and impaction of teeth 



were evidences, both in the tooth, in its bony surroundings, and in 
the external cortical bone, of the results of the irritation produced 



Fig. 88 




Impacted bicuspid. (Radiograph by E. Ballard Lodge.) 

by the efforts at eruption. The cementum was thickened; the outer 
follicular wall, the tissue designed to form the alveolar periosteum, 



Fig. 89 




Same as shown in Fig. 84, with tooth removed. (Cryer.) 



had exercised its formative osteogenetic function, and a capsule of 
bone had formed about the tooth; it lay in a bony chamber. The 



IMPACTED AND ENCYSTED TEETH 



121 



pressure exerted upon the distal wall of the second molar had resulted 
in a pressure resorption of its root until the pulp chamber was 
encroached upon. These were both postmortem cases, and no records 



Fig. 90 




Wisdom teeth embedded in the rami of the lower jaw. (Tomes.) 



of their clinical histories were obtainable. The symptoms produced 

could only be surmised by the nature of the anatomical relations 

and the pathological evidences. There may have been a prolonged 

but mild periostitis, probably a 

continued pulp irritation; and in FlG - 91 

the last, neuralgia of any grade /' i 

of severity. The pressure upon 

nerves of the inferior dental canal 

would account for neuralgia or 

mental or other disturbance. 

Oyer calls attention to the 
fact that a third lower molar in 
its attempt to erupt, frequently 
causes a cellulitis, extending into 
the temporomandibular joint, 
causing acute ankylosis. 1 

Instead of remaining in the 
alveolar portion of the bone, 
the impacted tooth may come, 
to occupy a cavity in some por- 
tion of the body or the ramus 
of the bone (Figs. 91 and 92). 
The positions of the teeth in 
such cases tend to confirm Tomes' s theory of the development of 
the jaw. The jaw being lengthened, and the ramus developing 




Wisdom tooth buried in the ramus. 
(Tomes, after Marshall.) 



1 Dental Cosmos, October, 1911. 



122 MALPOSITION AND IMPACTION OF TEETH 

through conjoined deposition and resorption of bone, the crown 
of the tooth appears to be either fixed in a bony nucleus and trans- 
ported to some distant point in the developmental progress of the 
jaw, or to be irregularly shifted about during jaw growth. At later 
periods, the pressure exercised by root formation disturbs the rela- 
tions of the tooth with its earlier surroundings. These efforts at 
eruption may, at late periods, cause the appearance of the tooth in 
odd situations. In the case shown in Fig. 92 the crown of the 
tooth made its way through the angle of. the bone and through the 
muscles and skin. The opening in the skin healed upon extraction 
of the tooth. 

Impacted Upper Third Molars. — Some phases of impaction of this 
tooth have been spoken of under the head of Pathological Dentition. 
The most common is imprisonment of the tooth and its subsequent 
partial eruption in a horizontal position, the crown pointing toward 

Fig. 92 




From a wax model in the museum of the London Odontological Society. (Tomes.) 

the cheek (Fig. 74). The crown of this tooth may, in rare cases, be 
directed inward or backward, in the latter case being arrested by 
the pterygoid plates of the sphenoid bone. It may present with 
an anterobuccal facing of the crown, as shown in Fig. 93, or with 
a posterobuccal facing. 

In a case recorded by Tomes (Fig. 94) the extraction of the 
second molar revealed the third molar in a reversed position, its 
roots occupying the depression between the roots of the second 
molar. A case has been reported, of an upper molar with the roots 
partly embedded in the floor of the antrum, its neck carious, 1 and 
the antrum in a state of suppuration. The upper third molar is 
liable to be joined to the second molar by concrescence (q. v.) and 
its descent prevented. 

1 Possibly resorbed or decalcified instead of carious. 



IMPACTED AND ENCYSTED TEETH 



123 



Impacted Cuspids. — In point of frequency of impaction the upper 
cuspids stand next to the lower third molars. The upper cuspids lie 
high up; the floors of their crypts, in which they lie loosely, are at a 
higher level than those of the adjoining teeth; their crowns, as with 
the other anterior teeth, lie lingual to the roots of their predecessors. 
All of these are elements which might cause displacement of the 
developing cuspids. Should the advance of eruption not keep pace 
with the development of the alveolar bone, imprisonment is likely; 
again, the dense bone immediately about the first bicuspid and 
lateral incisor may offer a deflecting resistance. Examining the 

texture of the bone about these 
FlG - 93 parts, it is evident that the 

direction of least resistance to 
the advance of a much deflected 
into the cancellated 




crown is 



Fig. 94 



Upper jaw, with the third molar directed 
forward and impinging upon the second 
molar. The small tooth situated high up 
in the anterior part of the jaw was forced 
there by the spade of the grave-digger. 
The artist's accuracy in delineating all 
parts of the specimen has rendered this 
explanation necessary. (Tomes.) 




A second molar of the upper jaw 
with the wisdom tooth inverted and 
embraced within the roots. (Tomes.) 



bone of the incisor portion of the alveolar process; hence it is most 
usual to find the crowns of these teeth lying with their cusps 
pointing forward (Fig. 95). Several recorded cases have the posi- 
tions shown; one or both of the teeth may be impacted. Cuspid teeth 
may erupt into the nasal cavity or appear in the canine fossa, and pre- 
sent the crowns cheekwise, or lie horizontally and above the roots of 
the bicuspids. 

Glas, of Vienna, discovered a cuspid in the nasal floor associated 
with calcic formations in its ulcerated surface (rhinolith). The 
patient, aged nineteen years, had frequent fetid eructations, with 
vomiting of green, foul-smelling masses. With the removal of the 
cuspid the vomiting, etc., ceased. 

A case of similar character producing antral empyema and a fistula 
upon the gum was due to an impacted supernumerary tooth. 1 



Crandall, Dental Cosmos, May, 1914. 



124 



MALPOSITION AND IMPACTION OF TEETH 



Impaction of Other Teeth. — While impactions are most common in 
connection with the teeth named, any other teeth of a denture may 
be imprisoned. Fig. 96 shows an impacted bicuspid whose root 




W 

Abnormal jaw, showing impacted cuspids. (Cryer.) 



Fig. 96 




Impacted bicuspid. (Salter.) 



development has been normal as regards its length, but whose curve 
has been modified by the resistance of surrounding tissues. Fig. 98 
exhibits an imprisoned central incisor, whose retention was, no 



IMPACTED AND ENCYSTED TEETH 
Fig. 97 



125 




Lower maxilla, in which the right second bicuspid is placed obliquely, the root being 
directed backward. The crown, though exposed, does not rise above the level of the 
alveolar margin. (Tomes.) 

Fig. 98 




Imprisoned central incisor. (Kirk and Cryer.) 
Fig. 99 




Maxilla, in which the temporary cuspids (the sockets of which are shown by the 
dotted lines) were retained, and the permanent canines developed within the substance 
of the jaw. The bone has been removed on the one side to show the direction taken 
by the tooth, which has been twisted on its axis to the extent of a quarter of a turn. 
(Tomes.) 




126 MALPOSITION AND IMPACTION OF TEETH 

doubt, determined and malposition caused by the development and 
presence of the brood of supernumerary teeth which surrounded its 
crown. 

Upper incisor teeth have been seen inverted and their crowns 
erupted into the nasal cavity, where they have produced inflammation, 
which later became infective. 1 A supernumerary tooth has been 
found in the floor of the nasal cavity 2 so that presence of all normal 
teeth should not exclude extra teeth from consideration in making 
a diagnosis. Radiography may demonstrate an unsuspected super- 
numerary. 

Impacted teeth do not necessarily produce such pathological con- 
ditions as produce untoward symptoms. The malposition of the 
impacted teeth either in total or partial impaction may, however, 
lead to malposition of other teeth, or results 
Fig. ioo such as caries. The relation of impacted 

teeth and any ulterior disease condition is 
settled by the facts, the probabilities of 
relation, or the results of their removal. 

Symptoms. — The most common symptom 
attendant upon impaction of teeth, judging 
from the obtainable records of cases, is tri- 
^^"olTZt facial neuralgia of any degree, caused by 
(Oyer.) impingement of the malposed tooth upon 

nerve filaments or trunks. Cryer 3 records a 
case where a supramaxillary neuralgia was traced to the presence of a 
central and lateral incisor, and a cuspid tooth in the anterior wall 
of the antrum; they were only discovered by an exploratory opera- 
tion. A cure of the neuralgia was effected by their removal. 

Impacted third molars frequently give rise to heavy rheumatic 
pains about the side of the face and jaws, and no doubt in such cases 
as depicted in Fig. 85 would cause intractable and diffuse maxillary 
neuralgia. Salter 4 records a case of long standing and intractable 
neuralgia, exhibiting a constant painful area upon the scalp, and in 
which heat and tenderness were noticed over a swelling upon the 
hard palate. Immediate and permanent cessation of the neuralgia 
followed removal of the teeth. 

Dr. N. T. Shields 5 describes a case of great pain in the region of 
the mental foramen, accompanied by a later appearance of fever, 
reaching 103.8°, with subsequent enlargement of the submaxillary 

1 Jameson: International Dental Journal, 1899. 

2 Boral: See Cosmos, December, 1911. 

3 Dental Cosmos, 1896. 
* Dental Pathology and Surgery. 
« Dental Cosmos, 1908, 



IMPACTED AND ENCYSTED TEETH 



127 



gland, as cured by the surgical removal of the two impacted bicuspids 
and deciduous tooth shown in Fig. 101. 

Symptoms of maxillary periostitis — heavy, gnawing, and dull, 
throbbing pain, with more or less heat and engorgement of tissues — 
are noted as an accompaniment of impacted teeth. Such symptoms 
may herald the appearance of the tip of the tooth through its bony 
covering and gum. 

Fig. 101 




Radiograph showing impacted teeth. (Shields.) 



Cases of maxillary abscess, in the absence of their usual cause 
(gangrenous pulp), may run a prolonged and painful course, 1 involv- 
ing neighboring structures, which may be vital, and after free venting 
be found to have arisen about an impacted tooth. The probable 

1 See Garretson's Oral Surgery and Salter's Dental Pathology. 



128 MALPOSITION AND IMPACTION OF TEETH 

explanation for many cases is the partial absorption of the overlying 
tissues, permitting ingress of bacteria, but in some cases crown 
resorption may cause irritation, and bacteria in the blood may 
localize. A few cases of pulp exposure have been seen when a sinus 
allowed ingress of bacteria and the production of caries. In such 
case a pulp may die, undergo putresence, and cause apical abscess 
with its symptoms. 

In some cases the pus travels from about the impacted tooth to 
distant parts, as through the musculature of the neck to the clavicle. 1 

Occasionally a circumscribed swelling is noted upon some aspect 
of a jaw, most frequently upon the palatal portion of the superior 
maxilla, which is attended by inflammatory symptoms, and an 
incision reveals an impacted tooth. If a plate has been worn, the 
tissue between, and even the bone may become necrotic. 

Fig. 102 Fig. 103 





X-ray photograph, showing mal- Impacted cuspid revealed by resorption 

posed cuspid entirely embedded in the of the overlying tissues. (Burchard.) 

bone and pressing upon the central. 

Quickly forming cysts of the jaw, upon receiving surgical treat- 
ment, may be found to contain the crown of an entire tooth, this 
evidently being the centre of irritation from which the cystic forma- 
tion had its origin. Melancholia, mania, and dementia precox have 
been relieved by the extraction of impacted teeth diagnosed by 
radiography. 2 This shows a relation between cause and effect (Fig. 
106). M. C. Smith 3 reports a case of lifelong attacks of prostrat- 
ing sick headache due to impaction of a third lower molar and 
relieved by its extraction. 

The pulps of other teeth have been devitalized by the strangula- 

1 Lyons: Jour. Nat. Dent. Assn., 1916, p. 33. 

2 Upson: Dental Cosmos, 1910, p. 527, 

3 Dental Brief, 1912. 




IMPACTED AND ENCYSTED TEETH 129 

tion due to the pressure of the crown of the impacted tooth upon 
the apical tissue, and the production of pulp nodules in other 
teeth through a reflex hyperemia has been noted. The resorption 
of roots of other teeth has been produced by the pressure of the 
impacted tooth. 

Hypercementosis and concrescence have also been produced by 
the descent of the tooth and have produced impaction. 

Resorption of the roots of the impacted teeth, or resorption of the 
enamel and dentin of the crown may occur. In one case, a calculus 
in nowise associated with the oral cavity, and divided from it by an 
area of pericemental tissue was found. (See Resorption of Enamel, 
for illustration.) 

In all these cases diagnostic features exist, though none are com- 
parable to radiography. 

Diagnosis. — Given symptoms not otherwise explainable or the 
absence of a tooth from the usual position, or both, an extraction or 
impaction is suspected, eliminating the first a radiograph is made. 

A tumefaction with a tooth absent from the arch is some evidence. 

Impacted teeth may become uncovered at some aspect late in 
life, and the condition be discovered incidentally. Cases are recorded 
where the pressure of a plate has caused the resorption of tissues 
overlying an impacted tooth, thus revealing its presence. Fig. 103 
illustrates a case where the presence of an impacted cuspid was 
revealed at the age of seventy years, through resorption of the 
alveolar bone and the gum tissue covering the tooth. 

Impacted molars with an opening leading, to them may be detected 
by instrumental exploration, or a sharp bistoury or exploring needle 
may be thrust through the gum and bone. 

As the smooth feel of enamel is a diagnostic feature when instru- 
mental examination is made, it is to be remembered that the enamel 
and dentin of an impacted tooth may undergo a true resorption 
with the characteristic Howship's lacunae. When partly exposed 
to the oral fluid,, caries may occur. Both these conditions produce 
rough surfaces, but enamel may usually be felt at some point. In 
all cases a radiograph is necessary to determine the position of the 
tooth and the steps necessary for its removal. 

Plate exposures may be best in obscure cases to determine a locality 
for further examination with a film exposure. (See Radiography.) 

Treatment. — The treatment of cases of impaction is ordinarily the 
removal of the offending tooth. When the tooth is embedded deeply 
in the substance of the jaw, access to it involves conductive anesthesia, 
and the removal of the bone which obstructs the path of extraction; 
this may be an operation of some magnitude, and is usually done by 
9 



130 MALPOSITION AND IMPACTION OF TEETH 

a special surgical practitioner. When, however, it is evident that 
the obstructions to the removal of the tooth consist of the soft 
tissues and but a lamina of bone, the operation for removal is clearly 
within the province of the dental operator. For example, the pres- 
ence of an impacted cuspid is determined, lying horizontally along 
the lateral aspect of the roof of the mouth. The parts may be 

Fig. 104 Fig. 105 





Impacted lower third molar; cause of Cuspid tooth, unsuspected by patient; 

neuralgia. (Radiograph by Lodge.) demonstrated to have been responsible 

for severe neuralgias. Patient, a 
draughtsman, had not been able to 
work at his business for the six months 
previous. The tooth was not known 
to be present, until revealed by x-rays. 
It was removed from the Ungual side. 
(Radiograph by Lodge.) 

Fig. 106 




Impaction of upper third molar, without local pain, cause of profound delusions and 
melancholia. (Upson. 1 ) 

injected with a local anesthetic solution, and a cut made with a 
sharp bistoury through the soft tissues from the outside of the 
swelling, to the bone. The flap thus outlined is raised from the 
bone, the flap including the periosteum. A large, sharp bur is then 
employed to remove the covering bone. When the tooth is freely 

1 Insanity Caused by Painless Dental Disease, Dental Cosmos, 1910. 



IMPACTED AND ENCYSTED TEETH 131 

exposed it may be dislodged with forceps or elevator. The parts 
are then washed with normal salt solution, dried, the flap pressed 
back into place, and steresol 1 painted over the parts, or a stitch or 
two of sterile horsehair may be taken before application of the steresol. 
The operation should be done under aseptic precaution and the 
mouth should of course be kept as aseptic as possible before and 
after operation. A simple clot kept aseptic may be sufficient. 

1$ — Purified gum lac gix 

Purified gum benzoin 5i 

Balsam of tolu 5 ^ 

Oil of cinnamon (Chinese) gi 

Carbolic acid 5iij 

Saccharin gi 

Alcohol Oij — M. 

1 Dental Cosmos, 1895. 



SECTION III. 

DEVELOPMENTAL ABNORMALITIES. 



CHAPTER V. 
MALFORMATIONS AND ANOMALIES OF THE TEETH. 

By malformation is meant either a microscopic abnormality in the 
histology of one or more tissues of a tooth or a developmental error 
which is plainly visible to the naked eye and often constitute a dis- 
tinctly abnormal tooth form or anomaly. The term anomaly also 
includes unusual peculiarities such as duplication, absence of teeth, 
etc., in which development has to be considered. When teeth are 
malformed through some abnormal developmental process which 
may be referred to an abnormal nutritional process the condition is 
termed a dystrophy, and when this is due to an arrested development 
the term hypoplasia is properly employed; the term atrophy in this 
connection is a misnomer as this is a lessening in a size previously 
attained through a process of normal nutrition. The lines cannot 
be sharply drawn as macroscopic appearances may require microscopy 
for their elucidation. 

For convenience the defects clearly microscopic will be classed as 
such while the more gross will be classed as macroscopic. 

As malformations of the parts about the mouth and of the teeth 
are dependent upon defective development of the same, it is incum- 
bent that certain facts concerning their embryology should be 
stated. In like manner, as the processes of pathology are modified 
by the peculiar anatomy of the teeth and associated parts, it is 
necessary that a previous knowledge of these be acquired before 
the special dental pathology can be comprehended. The embryo- 
logy of the mouth begins at a very early period — before the twelfth 
day the future mouth may be located (His, Fig. 107). The mouth 
and nasal cavity are circumscribed by parts which are developed by 
outgrowths from the head fold of the fetus. Those structures imme- 
diately concerned are the lateral tubercles arising from the frontal 
prominence (Fig. 108), which grow downward and fuse, forming the 

(133) 



134 MALFORMATIONS AND ANOMALIES OF THE TEETH 



nose, the nasal septum, the intermaxillary bones, and anterior portion 
of the upper lip (Figs. 109 and 110). From the sides of the head 
fold at the level of the mouth and neck appear certain lateral pro- 
tuberances, or pharyngeal 
arches. The first pharyngeal 
arches (Fig. 107, 4) divide into 
(1) the superior maxillary proc- 
esses (Fig. 107, 5) and (2) the 
inferior maxillary processes (Fig. 
107, 4, shown just beneath the 
oral cavity and united in the 
median line). 

The superior maxillary proc- 
esses develop the palate bones 
and the superior maxilla?. They 
form the balance of the upper 
lip. The arch itself forms the 
cheek. Fig 110, from a case of 
arrested development, illustrates 
the unions and parts naturally 
formed, but here incomplete. 

Face of an embryo of twenty-five to pj g> m m ^ch the Union of 
twenty-eight days (magnified fifteen times) : . 

1, frontal prominence; 2, 3, right and left the processes IS Still incomplete, 

olfactory fossae; 4, inferior maxillary tu- g } 10WS ^ ow ^^ an( J c J e f t pa l ate 
bercles, united m the middle line; 5, superior r 

maxillary tubercles; 6, mouth or fauces; 7, Can OCCUr. 

second pharyngeal arch; 8 third; 9, fourth; Secondary processes develop 
10, primitive ocular vesicle; 11, primitive . n i 

auditory vesicle. (Gray.) horizontally toward each other, 




Fig. 108 



Sup. tubercle 
Lateral tubercle 




Sup. tubercle 
Lateral tubercle 



Head of an early human embryo, showing the disposition of the facial fissures and 
the superior and lateral tubercles. (His.) 



MALFORMATIONS AND ANOMALIES OF THE TEETH 135 



S.M.P 




S.M.P. 



I.M. 



NAS. 



Diagram illustrating scheme of union of the processes: N.S., lateral tubercles 
forming internal maxillary bones, INT. MAX., and nasal septum; S.M.P., superior 
maxillary processes forming palatal processes of superior maxillae, S.M.P.; N.C., 
nasal cavity; O.C., oral cavity; I.M., inferior maxillary processes united. 



Fig. 110 




Complete bilateral fissures (coloboma) of face. (Guersant.) 



136 MALFORMATIONS AND ANOMALIES OF THE TEETH 

form the palatal portions of the superior maxillae and palate bones, and 
unite at the median line (Fig. 109, S.M.P., also Fig. Ill), forming the 
vault of the mouth and floor of the nasal cavity. Union occurs with 
the lateral processes, later forming the vomer and intermaxillary 
bones and bearing the germs of the incisor teeth (Fig. Ill), thus com- 
pleting the formation of the upper jaw and lip. 

Fig. Ill 




Vertical transverse section through head of human embryo, about the tenth week: 
1, nasal cartilage; 2, buccal cavity; 3, tongue; 4, dental ridge, lower jaw; 5, nasal 
cavity; 6, dental ridge, upper jaw; 7, dental ridge, lower jaw. X 30. (Broomell. 1 ) 



The inferior maxillary processes grow forward and unite at the 
median line, developing the inferior jaw and lip. Fig. 115, an arrested 
case, shows this. 

It is to be remembered that these processes are formed by the out- 
growth of the mesoblastic layer of the blastoderm, and are covered by 
epithelial tissue springing from the epiblast. Both are concerned in 
the formation of the teeth. Epithelium is reflected over the face and 
oral cavity. All tissues between these layers of epithelium excepting 
the dental band and enamel organs and the nerves are of mesoblastic 
origin. 

The structures of the floor of the mouth and neighboring structures 

1 Anatomy and Histology of the Mouth and Teeth. 



MALFORMATIONS AND ANOMALIES OF THE TEETH 137 

are formed from the second, third, and fourth pharyngeal arches and 
a tubercle arising near the first pharyngeal arch. The fusions of the 
lateral portions of the upper maxillae begin first anteriorly at about 



Fig. 112 



One for nasal and 
facial portions. 



One for orbital and 
malar portions. 



One for incisive 
portion. 



One for palatal 
portion. 




At birth. 



Inferior Surface. 

Development of the superior maxillary bone by four centers, also development of 
intermaxillary bones. (Gray.) 



Fig. 113 



Fig. 114 





Cleft of hard and soft palate; rudimen- 
tary intermaxillary bone placed in advance 
of lips. (Mason.) 



Cleft of hard and soft palate. 
(Mason.) 



the eighth week, and progress posteriorly until complete at about the 
eleventh. Malformations due to non-union, therefore, date from 
this period, and consist of the following typical varieties: 



13S MALFORMATIONS AND ANOMALIES OF THE TEETH 

1. Non-union of lip on one or both sides — simple hare-lip. 

2. Non-union of lip and of maxilla and intermaxillary bone on one 
side (hare-lip, Fig. 113). 

3. Non-union of lip and intermaxillary bone on both sides (double 
hare-lip, when complete bilateral fissures are formed it is termed 
Coloboma, Figs. Ill, 113, 114, 117). 

4. Non-union of all horizontal processes in the median line (cleft 
palate, Figs. 113 and 114). (It may be double, divided by the vomer, 
including the hard palate. 1 ) 

5. Non-union of halves of soft palate (cleft velum). (Usually 
involving part of the hard palate.) 

Fig. 115 




Median fissure of the lower lip and chin. (Marshall, after Wofler.) 

6. Non-union of halves of the uvula (bifid or cleft uvula). 

Combinations of cleft velum and cleft palate or of cleft palate and 
single or double hare-lip may exist. 

A case of failure of development of the intermaxillary bones has 
been reported, 2 the space between the cuspid teeth being about 
one-eighth inch. 

Figs. 110 to 114 show the parts in their ununited state. 

The failure of the inferior maxillary processes to unite is rare, 



1 Brown: Oral Diseases and Malformations. 

2 Jeffery, British Dental Journal, July, 1904. 



MALFORMATIONS AND ANOMALIES OF THE TEETH 139 

but is occasionally seen (Fig. 115). There is some evidence of heredi- 
tary influence in many cases. 1 The inferior maxillary tubercles 



Fig. 116 



Fig. 117 





Showing Meckel's cartilage (M.C.) in 
longitudinal and transverse section. 



Osteology of hare-lip. (Museum of the 
Philadelphia Dental College.) 



Fig. 118 




Section of jaw, embryo of pig, showing growth of enamel organ and dentin germ: 
1, enamel organ; 2, dentin germ; 3, growth of jaw; 4, tongue. (Andrews.) 

1 Brown: Oral Diseases and Malformations. Humphreys: Dental Cosmos, 1914, 
P. 44. Blades: Dental Cosmos, November, 1914. 



140 MALFORMATIONS AND ANOMALIES OF THE TEETH 

develop a transitory support to the lower jaw known as Meckel's 
cartilage. The cartilages of the right and left side do not fuse 
together at the future symphysis. (Hertwig.) (Figs. Ill and 116.) 
It acts as a support to the fetal jaw, undergoes atrophy at about 
the sixth month of gestation, and at birth but few fragments are 
found near the symphysis. At birth ossification has occurred, and 

Fig. 119 




Section of developing tooth of an embryo calf: a, stellate reticulum of enamel 
organ; b, stratum intermedium; c, ameloblasts; d, dentin; e, odontoblasts; /, blood- 
vessels — corpuscles in situ. X- 275. (Williams.) 

the bone consists of two halves united by a fibrous symphysis in 
which ossification takes place during the first year. 

The end of the cartilage in the base of the inferior-maxillary process 
becomes the future malleus (one of the bones of the middle ear). The 
portion of the cartilage running from the malleus to the formed bony 
lower jaw becomes transformed into the internal lateral ligament of 
the inferior maxilla. (Hertwig.) 



A 



MALFORMATIONS AND ANOMALIES OF THE TEETH 141 

We must keep in mind the foregoing facts and also the process of 
tooth development by the three formative organs. 

1. The enamel organ lined upon its under surface with amelo- 
blasts (Figs. 118 and 119), which deposit enamel as enamel globules 
cemented together by interprismatic cement substance, the two forming 
finally an enamel rod or prism. The rods are cemented together by 
the interprismatic cement substance (Fig. 121). 

Fig. 120 




Mode of enamel deposition: A, formed enamel; B, ameloblasts; C, secreting 
papillae of stratum intermedium; D, bloodvessels in external fibrous coat and to 
secreting papillae; E, enamel globules with connecting plasmic strings; F, nuclei 
of ameloblasts; G, blood supply of odontoblastic layer; H, odontoblasts; /, un- 
formed dentin; J, formed dentin. The interprismatic cement substance is shown as 
smaller bodies within the ameloblasts. Semidiagrammatic. (Williams.) 



2. The dentinal papilla (the dentin organ) covered upon its outer 
surface by odontoblasts (Figs. 118 and 119) which deposit dentin 
globules cemented together by dentinal cement substance, both exuded 
by odontoblasts (Mummery). The odontoblasts leave portions of 
themselves within the dentinal tubules constructed by themselves, 
these tubes lying within a general dentinal substance known as 



142 MALFORMATIONS AND ANOMALIES OF THE TEETH 

iritertvbvlar substance. The result of this mode of development of 
dentin is nicely shown in Figs. 122 and 123. 

Fig. 121 




Section of enamel of human tooth. Photographed with Zeiss apochromatic lens 
and Powel and Leland apochromatic condenser. The optical parts accurately centred 
and the focus "critical." The enamel rods are seen to be resolved into distinct sec- 
tions (enamel globules), the cement substance often passing entirely between the 
sections. X 400. (Williams.) 

Fig. 122 




—T-V 2 



Transverse ground section through the dentinal tubules of the first molar of a child 
aged seven years: V, small connecting tubule. Koch's and Golgi's methods combined, 
X 1200. (Rose.) 



MICROSCOPIC MALFORMATIONS 143 

3. The follicle wall (the cement organ) and later the pericementum, 
a fibrovascular membrane containing on its inner and outer surfaces 
osteoblasts which form respectively the cementum of the root as a 
modified bone and the alveolar wall. It completely encircles the 
enamel organ and papilla and any of their products and with its 
enclosures constitutes the dental Jollicle. It is upon aberrations in 
these three organs that dystrophies and anomalies of teeth depend. 

Fig. 123 




Main mass of dentin of a temporary tooth, stained with chlorid of gold, decalcified 
with acetic acid: F, F, dentinal fibers, partly vacuolated; B, B, basic substance, 
traversed by a reticulum. X 1200. (Hart.) 



MICROSCOPIC MALFORMATIONS. 

Microscopic or histological defects may affect any of the dental 
tissues, enamel, dentin, cementum, pulp, or pericementum. 

Enamel. — Defects in enamel structures range from any degree of 
orderliness in the even distribution of globular bodies and cementing 
substance in the tissue, to gross aberrations in formation. The finer 
variations of structure are not easily recognizable. 

Theoretically perfect enamel should show in longitudinal section a 
series of squares of uniform size built into rods, the outlines of 
the squares and rods being marked by lines of cementing substance 
having a refractive index slightly different from that of the squares 



144 MALFORMATIONS AND ANOMALIES OF THE TEETH 

(Fig. 121). While such a structure is perhaps never found, it is 
difficult to draw a line where aberrations from such a standard become 
pathological. An arbitrary standard might be assumed as follows: 
Regard any enamel as pathological, where areas of it differ from its 
general substance to such an extent as to have a decidedly different 
refractive index. A typical form of abnormality is noted in what 
are known as opaque spots in the enamel, areas in which an opaque 
surface exists instead of the normally translucent enamel. 

Fig. 124 




Section of human molar, showing dentinal fibrillae penetrating enamel. X 600. 

(Williams. 1 ) 



Dentinal Fibrils in Enamel. — The dentinal fibrillae may penetrate 
the substance of the enamel (Fig. 124), occupying defined channels 

1 For an interesting article illustrating this point see Boedecker, Dental Cosmos, 
1911, p. 1000. 



MICROSCOPIC MALFORMATIONS 



145 



in its substance; this was formerly regarded as a developmental 
accident. Caush 1 claims to have found this to be a normal condi- 
tion of human enamel, and regards these as nutrient spaces. Still 
later Boedecker has found them to frequently occur in enamel (Fig. 
126). Andrews 2 states that "examination of sections at the junc- 
tion of formed dentin and ameloblasts show fibers span any space 
formed between them." Evidently there must have occurred a 
mixture of the elements of dentin and enamel, the record showing an 

Fig. 125 




Section of human incisor, showing "bands of Retzius" and marked stratification of 
enamel. X 125. (Williams.) 

interdigitation of papilla (probably odontoblasts) and enamel organ 
(probably ameloblasts) . After calcification these odontoblastic fibers 
are caught in the enamel. Von Beust also has experimentally shown 
this (Fig. 126). Gies 3 injected trypan blue into the peritoneal cavity 
of animals and found it in the pulp, dentin and to an extent in the 
enamel. Such conditions are not to be confounded with fissures of 
enamel where large lines of faulty calcification or non-calcification 



1 International Dental Journal, June, 1904. 

2 Dental Cosmos. 1912, p. 49. 

3 Journal of Allied Dental Societies, September, 



1914, 



10 



14G MALFORMATIONS AND ANOMALIES OF THE TEETH 

Fig. 126 




Injected tooth, showing connection between dentinal tubules and enamel tubes. 

(von Beust.) 



Fig. 127 




Specimen of decalcified adult enamel, showing enamel prism sheaths and lamella (L) 
put longitudinally. X 500. (Boedecker.) A 



MICROSCOPIC MALFORMATIONS 



147 



extend through the thickness of enamel. A portion of the enamel 
may occupy an area within the dentin. This in itself shows that the 
enamel and dentin organs can be heterogeneously arranged. An 
odontoma is another evidence. 

Enamel, even normal enamel, is not of uniform composition; were 
it so, it would exhibit, in addition to an orderly arrangement of its 
histological elements, a uniformity in color. So common are differ- 
ences in this direction that the presence of pigment bands must be 
regarded as normal. It is the rule to find enamel traversed by deeply 
pigmented parallel bands, which pass obliquely upward from the 
surface of the dentin to the surface of the enamel. These are termed 
the bands of Retzius; they appear to mark the size of the enamel 
cap at successive periods of its growth (Fig. 125). 

Fig. 128 




Injected tooth, showing connection between dentinal tubules and lacunae of 
cementum. (von Beust.) 



Stratification and striation of the enamel, as shown by Williams, 
must be regarded as normal physiological records of the mode of 
enamel formation. Kirk has shown that normal enamel shows vari- 
ations in density in the same teeth. 

All of these histological defects represent variations of deposition, 
no doubt due to fluctuation of the nutritive processes of the child at 
the time of tooth formation. Histological records made in the enamel 
are not like those made in other tissues, for there is no certain pro- 
vision through which such defects can be remedied at subsequent 
periods. 



US MALFORMATIONS AND ANOMALIES OF THE TEETH 

Profound nutritive disturbances, such as those attending hereditary 
syphilis in children, affect the structures of the teeth. One of the 
gross results of this disease is a common malformation of the general 
form of the incisors. The hard tissues of such teeth exhibit micro- 
scopic evidences of faulty histology; they are dull and opaque, and 
traversed by irregular bands. Viewed in section, the enamel of such 
teeth is seen to be almost structureless (Fig. 129). Williams found 
that the contents of the large, irregular spaces in this enamel did not 
respond to stains — i. e., did not contain organic matter. Such teeth, 
when not presenting gross malformations, may have a distinct irregu- 
larity of enamel surface. This may even be seen with the naked eye, 
or graphite may be rubbed over the teeth, bringing out the lines. 

Fig. 129 




Section of enamel from syphilitic tooth, with appearances resembling the lacuna? of 
cementum. X 600. (Williams.) 

Among the poor children in clinical service opacity of enamel is 
frequently noted, whether this is due to syphilis or to general nutritive 
disturbances was not investigated, but in view of the available 
evidence it would seem most just to attribute it to abnormal nutri- 
tion. 1 As a prophylactic measure breast feeding of the child and ample 
nutrition of the parent and child seems the indication if applicable. 

Stripes of Schreger. — Cloud-like markings are also seen in enamel, 
which are called the stripes of Schreger. They run from dentin 

1 See Structure as Predisposing Cause of Dental Caries. 



II 



MICROSCOPIC MALFORMATIONS 



149 



toward the periphery, and are considered by Pickerill to be due to an 
optical effect produced by superimposed prisms 1 (Fig. 130). 

Lodge, 2 in an investigation of this subject, found that if a section 
of enamel was made at an angle of 45 degrees to the axis of the prisms 
the optical effect recognized as Schreger's bands and which ordinarily 
are seen only at the dentinal tw T o-thirds can then be seen running 
entirely to the periphery. He further states that the structure of 
teeth susceptible to caries renders the refractive indices of the prisms 
unequal and therefore more likely to produce the cloud effect. He 

Fig. 130 




Enamel and dentin, human tooth: 1, enamel; 2, dentin; 1, lines of Schreger in 
enamel; 4, brown striae of Retzius. (Probably aggregation of tubes, editor.) (Broomell, 
after Geise.) 

deduces that enamel of perfect quality would account by its equal 
light refraction of the prisms for specimens cut at 45 degrees to axis 
and lacking the stripes of Schreger. 

"With reflected light only the lines appear of a bluish or slaty color, 
the intervening areas white — with a small admixture of substage 
light the dark bands are areas of considerable translucency and the 
intervening areas opaque white." He is therefore in accord with 
those who agree upon an optical effect as the cause of these phe- 



1 Pickerill, Dental Cosmos, October, 1913. 

2 Dental Cosmos, November, 1917. 



150 MALFORMATIONS AND ANOMALIES OF THE TEEfti 

nomena, and as they are in effect superimposition of a net-like 
structure, he proposes the rational term "reticulum lines." 

There is evidence that other forms of specific dermatitis — scarlet 
fever and measles — which occur at an early age may affect the 
formation of enamel. The gross defects attributed to the exan- 
themata are irregular pits upon the crowns of, particularly, the 
incisors (Fig. 141, etc.), though other teeth also suffer. In some 
cases the crowns appear honeycombed. The condition is known as 
hypoplasia of the enamel, and is evidently- due to an effect upon the 
enamel organs. The microscopic structure is also affected. There 
is evidence in some specimens (Fig. 148) that the dentin may 
be hypoplastic; the papilla being doubtless affected by the pre- 

Fig. 131 




Lines of Schreger in the enamel of a permanent and deciduous tooth (human). 
Bulge of enamel at cervix of deciduous tooth is shown due to bulging of dentin, not 
to thickness of enamel. (Pickerill.) 

vailing systemic malnutrition. The dentin being first developed, 
shows perhaps normal for a distance, then a row of interglobular 
spaces is found, which is evidence that the dentin organ is affected 
by the general disturbance at the same time as the enamel organ. 

Hopewell-Smith 1 describes the enamel developed during rickets as 
faulty, and, in so far as limited observation could determine, con- 
tained numerous spaces probably filled with soft tissue. These 
spaces were in the first-formed portions of the specimens observed. 

Dentin. — Data regarding the finer phases of defective histological 
structure of the dentin are meagre. It has been observed that the 

1 Loc . cit. 






MICROSCOPIC MALFORMATIONS 151 

dentinal tubuli of some teeth are much larger than in others of the 
same age, and, no doubt, future investigations with an improved 
technique directed toward a study of the exact mode of dentin 
formation will exhibit defects more certainly. 

The chief histological defects noted in dentin are areas of faulty 
or non-calcification, called interglobular spaces (Fig. 132). These 
are most common in the dentin immediately underlying its covering 
tissue; so common in the dentin under the cementum that this 
portion of dentin has been called the stratum granulosum, the 
granular layer of Tomes (Fig. 134). In the body of the dentin these 
spaces have a more irregular distribution. 

Fig. 132 




Section showing interglobular spaces in dentin of a syphilitic human tooth. (Williams.) 

In wet-ground sections (Rose) the dentinal filaments are seen to 
pursue an unbroken course through these areas. The contents of the 
interglobular spaces react to stains like the sheaths of Neumann; 
that is, they probably contain transitional tissue. These areas 
probably represent, as do defective spots of enamel, periods of 
depressed vitality, or of altered nutrition. In the light of present 
knowledge regarding the subject, they are to be viewed as areas in 
which calcification was faulty. 

Interglobular spaces afford some evidence of the formation of 
dentin by a deposition of globular bodies in a matrix of protoplasmic 



152 MALFORMATIONS AND ANOMALIES OF THE TEETH 

Fig. 133 



^^^HH 




** 



Interglobular spaces crossed by dentinal tubes. Prepared by Weil's process. Magnified 
240 times. (Hopewell-Smith.) 








Ground section through the root of a human premolar: D, dentin; K, cement 
corpuscles; 0, osteoblasts; Ep, remains of Hertwig's epithelial root sheath or peri- 
cemental glands of Black : a J. interglobular spaces. X 200. (Rose.) 



MICROSCOPIC MALFORMATIONS 
Fig. 135 



153 




4 



Schreger's lines in dentin. From the ivory of the tusk of a walrus. Prepared by 
grinding. Unstained. X 45. (Hopewell-Smith.) 



Fig. 136 




J 



The same as Fig. 135. X 420. (Hopewell-Smith.) 



15-i MALFORMATIONS AND ANOMALIES OF THE TEETH 

material. The continuation of the tubules through the mass of 
uncalcified contents is evidence of their probable independent for- 
mation by special fibril cells as claimed by Andrews. 

Occasionally lines appear in dentin at a common developmental 
level and having a degree of parallelism to the pulp surface. They 
are evidently records of a new period of increment and consist of 
short curves in the tubules. They are called contour lines of Owen, 
also lines of Schreger in dentin (Figs. 135 and 136). 

Histological malformations of the pulp have not been recorded, the 
normal histology of the organ not being made out with sufficient 
certainty to determine what appearances are to be regarded as 
abnormal. Aberrations in form of pulp cavities are constant. 

Fig. 137 



-- - < ~::rr-- - \.-, -^ J^ __ v 




Section of a bicuspid with its alveolus, showing a pit-like absorption upon the side 
of the root in which the redeposit of the cementum has begun: a, dentin; 6, cementum; 
c, peridental membrane; d, bone forming the wall of the alveolus; e, absorbed area of 
cementum. It will be noticed that a new deposit of cementum has begun the filling 
of the area, and that the soft tissue in the area of absorption is of a cellular type. The 
bone also shows the effects of absorption in the cutting away of portions of the ring 
of the Haversian systems at/, while at g the presence of osteoclasts shows that absorp- 
tion is in progress at that point. (Black.) 



Cementum. — The pericementum may contain numbers of mul- 
tinucleated cells — odontoclasts; and their presence is not to 
be regarded as abnormal. The cementum of the roots of teeth 
may exhibit evidences of former action of these cells in excava- 
tions of cementum, which, by a subsequent deposition of cemen- 
tum, have become filled. This gives an irregular course to the 
cement laminae (Fig. 137). These appearances are to be regarded 
as not necessarily pathological, for the following reason: for some 
time (years) subsequent to the eruption of the teeth, developmental 
changes occur in the alveolar bones; depositions (subperiosteal) 






MACROSCOPIC MALFORMATIONS 155 

increasing their volume are accompanied by resorption of other 
portions of the bone, such a balance being kept between their proc- 
esses that the teeth, although shifting their positions, are kept in 
normal occlusion. 

The cementum may be thickened by additional deposits, as in 
hypercementosis, which is an excess of development classed as 
pathological. 

MACROSCOPIC MALFORMATIONS. 

Under this heading two subdivisions will be made: 

1. Dystrophies of the teeth. 

2. Anomalies of development not of dystrophic character. 
Dystrophies of the Teeth. — There are several forms of macroscopic 

malformation which seem due to disturbances of function or nutrition 
of the developmental organs and this in turn apparently caused by 
some severe general disturbance notably the exanthemata classing 
syphilis with these. 

Opaque Spots in Enamel. — White, brown, and corn-colored opaque 
areas of enamel are frequently seen, surrounded by apparently normal 
enamel. 

Examined without the aid of the microscope they are seen to 
present a surface as smooth as any enamel, though sometimes slightly 
crenated, but upon this surface being broken up with a bur a chalky, 
granular, whitish material containing at times the yellowish pigment 
is seen, sometimes occupying the entire thickness of the enamel. 
These spots, if slight, are sometimes without this granular character, 
while the pigment affects the entire thickness of the affected enamel. 

Williams submitted the enamel at the borders of such spots to 
microscopic examination, and compared it with enamel in the first 
stages of decay, finding in both a similar appearance, characteristic 
of a lack of, or a loss of interprismatic cement substance (Fig. 138). 

Mottled Enamel. — H. A. Flynn 1 called attention to the prevalence 
of opaque enamel in 87 per cent, of children born and raised in 
Colorado Springs while only sparingly found in other nearby localities. 

This condition has been shown to exist in various localities in about 
this percentage and confined to them. It is therefore an endemic 
condition. Black and McKay 2 in an exhaustive investigation of this 
condition published the following conclusions: 

1. The mottled teeth are found only in the groups of permanent 
teeth subjected to the influence of the local conditions while the 
enamel is developing and the temporary teeth are not affected. 

1 Items of Interest, 1910. 

2 Dental Cosmos, February to August, 1916, and Journal of Nat. Dent. Assn., 
July, 1918 and April, 1919. 



156 MALFORMATIONS AND ANOMALIES OF THE TEETH 

2. The lingual surfaces are opaque, paper white, mottled, with nor- 
mal spots and clouded areas. The labials are opaque, paper white, 
mottled with brown spots or brown or black bands. The surface 
glaze was present. 

3. The general form of the teeth was normal, though in a few 
cases hyperplasias were also present probably having no causal 
relations (McKay). 

Fig. 138 



'*§ ** 









-* 






Portion of a white spot in enamel, showing lack of interprismatic cement substance. 

X 2000. (Williams.) 



4. The enamel rods were well formed but the interprismatic cement 
substance was replaced by a brown colorirg pigment in the dark 
colored areas (called brownin by Black), but no cement substance 
was found in the opaque white areas. Only the superficial layers of 
enamel were affected. The yellow shades were due to brownin 
within the substance of the enamel and showing through more 
translucent enamel above it. The brownin appears in about 40 per 
cent, of the mottled cases. 

5. The brownin can be dissolved out by immersing in absolute 



MACROSCOPIC MALFORMATIONS 



157 



alcohol (four days) followed by immersion in gasoline (one month) 
and the resulting opaque white tooth can be permeated with stains. 

6. The condition is endemic to certain localities but may appear 
in children taken to such localities in the period of life during which 
the permanent teeth are developing. It is occasionally exceptionally 
found in other localities and it may exist on a few teeth only. 

7. The teeth erupt in the mottled state but the coloring makes its 
appearance some time later. It is not certain whether this pigment 
is laid in before eruption or is an infiltration of some exterior sub- 
stance. 1 The lower incisors while mottled are rarely stained. 

Fig. 139 




Mottled enamel. (McKay, Dental Cosmos.) 



8. All factors except residence in the endemic region during enamel 
formation may be excluded. Removal from the endemic district 
after damage does not remove the discolorations while removal for a 
part of each year during enamel formation seems to exercise an 
inhibitive influence upon the lesion. 

9. Exhaustive analyses of the drinking water showed no constant 
relation between the lime or other content and the prevalence of the 
lesion nor could artificial feeding in infancy be related with it. There- 
fore the cause remains obscure though later investigations seem to 
show that artesian water is probably most often the source of the 
drinking water, as in several endemic districts, native children 
raised on such water had mottled teeth, while native children using 
dug well (surface) water were free from the affection. 

1 McKay, Jour, N»& Pent, Assn,, 1917, p. 274. 



158 MALFORMATIONS AND ANOMALIES OF THE TEETH 

It is remarkable that the first formed enamel is normal while 
that later formed is abnormal yet the water drinking is constant. 
The difference between this condition and rickets which affects the 
early formed enamel is also notable (see Fig. 139). 

McKay, arguing against syphilis as a cause, points out that 
nearby localities may be afflicted or not, which syphilis would not 
accomplish. The treatment of mottled enamel consists in the 
removal by grinding of the outer layer of enamel with subsequent 
polishing. 

Fig. 140 




Section through human cuspid, showing sulcus and appearance of tissue in its vicinity 
X 75. (Specimen by Choquet; photograph by Williams.) 

In one case of an adult lady, a broad, brown spot was seen on 
a lower left lateral. There was a history of the temporary lateral 
having been knocked out. The writer has a Philadelphia patient 
who has the labials of the upper incisors each marked with a broad 
white spot in the center of which is a large brown. No history as to 
the water drunk is obtainable. While the endemic regions show the 
condition prevalent, it is not clear that the defect is distinct from 
the opaque spots mentioned on page 155 except as to cause. 

Hypoplasia of the Dental Structures. — By hypoplasia in this 
connection is meant an arrested development of any portion of a 
tooth. Necessarily the tooth is deformed. 



II 



MACROSCOPIC MALFORMATIONS 



159 



The term atrophy has been used in this sense, but is better 
confined to a lessening in size after normal development of a part has 
occurred. Nutritional disturbances, the exanthemata, and syphilis 
all seem to have a profound influence upon the form of teeth develop- 
ing during the period of active disease, by affecting the cells of 
the formative organs. With the passing of this period, the develop- 
ment of the tooth niay proceed in an orderly manner. The fol- 
lowing forms of hypoplasia are known: 



Fig. 141 



Fig. 142 





Hypoplasia due to eruptive fevers. 



Agenesis of incisal portion of enamel. 



Pitted and Grooved Teeth. — The hypoplasias described under this 
heading may consist of a series of irregular grooves or pittings, the 
crowns having approximately the normal outlines. Of these malfor- 
mations Figs. 141 to 146 are fairly typical. 



Fig. 143 



Fig. 144 





Showing the front teeth grooved from the alternation of perfectly and imperfectly 
developed portions of enamel. Hypoplasia. (Tomes.) 



Black regards the formation of pits, the simultaneously developed 
zone of enamel being perfect, as due to aberration in development of 
enamel rods, leaving a hole (doubtless a localized effect upon the 
ameloblasts). Histologically the strata of the enamel partly fail of 
deposition at these points (Fig. 141). The malformation follows 
the striae of Retzius. 

With a history of a case, including the age of the child at the period 
of the disease, if examination be made of the positions of the defects, 
the age will serve as an indication as to whether there has been any 



160 MALFORMATIONS AND ANOMALIES OF THE TEETH 

connection between the eruptive fever and the dental malformation. 
For example, if .enamel pits upon incisors have been caused by an 
eruptive fever between the ages of four and five, they should occupy 
a part a little above the half-way area of the crown face of a central 
incisor. The lateral will be affected nearer the incisal edge and the 
cuspid still more so; it is evident that the enamel being already 
formed about the incisal edge of the tooth, alterations of nutrition 
could not affect the already formed tissue. (See Fig. 50.) The 
enamel formed after a period of attack may be perfect (Fig. 145). 

Hutchinson's Teeth (Hypoplasia). — During the first few weeks 
after birth, skin eruptions characteristic of hereditary syphilis are 
apt to occur in the contaminated child. At this period the tips of 
the permanent incisors are undergoing development, the first per- 
manent molar having started at the twenty-fifth week of gestation 
(see Fig. 50), and the effect of the syphilitic eruption, during which 

Fig. 145 




Malformations of incisal half of crowns, with cervical half perfect. Hypoplasia. 
(Model by W. A. Capon.) 

the protozoon treponema pallidum may be in the enamel organ (or 
there is a severe disturbance of metabolism brought about by the 
infection, according to the preferred view of Stein 1 ), is to cause 
a disturbance of the enamel organ and papilla, which produces a 
defective development at this point. Instead of the normal angles 
and flattened curves of the labial surfaces, the incisors may have 
a roughly rounded and stunted appearance. The incisal edge of 
the tooth is narrower than its neck. The enamel at this edge is 
irregularly and badly formed; but there is a semblance of the three 
enamel tubercles found normally. The middle tubercle, being com- 
posed of defective enamel, is soon lost by abrasion, causing the 
tooth to have a notched appearance (Fig. 147). Stein quotes an 

1 Dental Cosmos, July, 1913, p. 693, 



MACROSCOPIC MALFORMATIONS 



161 



old authority as having seen one central notched and the other 
normal. The first permanent molars are often exceedingly corru- 



Fig. 146 




Pitted and fringed teeth, some of them carious at the incisal edges. Specimen in 
museum of Philadelphia Dental College. 

Fig. 147 



****mm^ 



Hutchinson's teeth. Hypoplasia. Two upper centrals notched and contracted. 
Characteristically undeveloped upper jaw. From a hereditary syphilitic, aged 
twelve years. 

gated and pitted, the pits extending into the dentin. These pits 
often decay, the points are broken or worn away, sometimes leaving 
a discolored, often black surface. (Fig. 151.) 
11 



102 MALFORMATIONS AND ANOMALIES OF THE TEETH 

In an exhaustive treatise upon this subject, Cavallaro 1 has shown 
that the pitted cuspal deformity of the first molars, the notched 

Fig. 148 




Hypoplasia of enamel, showing arrested stratification; dentine shows effects of hypo- 
plasia at interglobular spaces. (Hopewell-Smith.) 



incisors of Hutchinson, and the dystrophic cusps of canines in the 
permanent set, as well as similar effects occurring in the temporary 



Fig. 149 




Syphilitic teeth in upper and lower jaws 
as they appear when recently erupted. 



Fig. 150 



mwm 



The teeth of hereditary syphilis at 
maturity. 



set, are the stigmata of hereditary syphilis, either direct or in the 
second generation. He found the treponema pallidum in the dental 
follicles of syphilitic fetuses. 



Dental Cosmos, 1908. 



. 



MACROSCOPIC MALFORMATIONS 



163 



He calls attention to the possible effect upon the first molar enamel 
(developing before birth) alone, as indicating the cessation of tre- 
ponemal activity, though the incisor enamel (developing after birth) 
is usually affected. The cuspid (developing still later) may not be 
affected; which shows a cessation of germ activity between incisor 
and cuspid development. The dental stigmata may thus occur in 
the absence of the under-developed body and other physical charac- 
teristics of syphilis, though these may also be in evidence, as well as a 
history or evidence of more or less active manifestations of syphilis. 1 

Fig. 151 




Semidiagrammatic representation of a systematized hypoplasia of several kinds of 
upper and lower teeth. The general systemic disturbance which must have caused 
these stigmata, commenced about the twenty-fifth week of intra-uterine life and con- 
tinued up to about the fourth month after birth. (The third molars omitted.) 
(Stein.) 



Stein 2 argues that as the stigmata are bilateral and symmetrical, 
they could not have been produced by causes acting locally, but 
that the general disturbance of metabolism affecting the develop- 

1 No matter what conviction a dentist has that these dystrophies are of syphilitic 
origin, he must be cautious regarding the expression of his opinion. Even the thought- 
less leaving of a copy of this volume upon the desk from which it was picked up and 
this chapter seen by a lady patient, produced questions of a very embarrassing character, 
regarding certain defects in her child's teeth. Unfortunately, Cavallaro's investi- 
gations do not take sufficient cognizance of the possible intervention of other exanthe- 
mata, either in the subject or mother; for example, in his Case XX, a girl, aged four- 
teen years, hereditary syphilitic showing transverse grooves in the teeth, the effects 
are attributed to syphilis. The child may easily have had other complications, such 
as measles. Stein excludes rachitis, variola, scarlatina, diphtheria, typhoid and 
rheumatism as very rare possible causes of the hypoplasia. 

2 Dental Cosmos, July, 1913, p. 695. 



164 MALFORMATIONS AND ANOMALIES OF THE TEETH 

mental organs of the teeth causes interference with the functions 
of such of them as should be actively developing tooth structure. 

While to syphilis, may now be accredited much of the pittings upon 
teeth, the history of an attack of one of the exanthemata, such as 
scarlet fever or measles, at a certain age corresponding to the devel- 
opment of the particular part of the tooth which has undergone 
hyperplasia makes it rational to accredit the effect to such exanthema. 
Measles often causes characteristic eruptions in the mucous mem- 
brane of the mouth and pharynx, and could easily affect the dental 
follicle. If the disease and the effect do not correspond chronologic- 
ally they should not be related. Syphilis is in a way, an exanthem- 
atous disease of chronic nature. 

In hereditary syphilitics, Cavallaro found the following dental 
stigmata: Hypoplastic defects of systematic character with predi- 
lection for the central incisor forming the notched incisor or Hutchin- 
son's tooth, and also cuspal defects, white sulci, white marks, delay 
of development and eruption, dental infantilism, microdontism, 
amorphism, persistence of deciduous teeth, cuspal defects of decidu- 
ous teeth, especially the second molar, anomalies of structure, 
shape, number, direction, arrangement, and color, vulnerability of 
the dental system, ectopia, total or partial absence of teeth, wearing 
away, premature caries, premature loss of teeth, space between teeth, 
diastema. Also the following maxillary stigmata: malocclusion, 
defective articulation of the dental arches, prognathism, ogival 
palate and cleft palate. 

Stein offers the following perhaps more clearly expressed classi- 
fication: 

"1. Multiple disseminated stigmata of the teeth, both in the 
maxilla and the mandible. 

2. Symmetrical stigmata here and there upon homologous teeth. 

3. Systematized stigmata at the same level on teeth of the same 
kind, but at a different level on different kinds of teeth. 

The most characteristic stigmata of the teeth of heredosyphilis 
are: 

1. Hypoplasia of the four first molars. 

2. A systematized hypoplasia upon the several upper and lower 
teeth. 

3. Hutchinson's teeth. Microdontism and non-replacement of 
deciduous teeth due to arrested development of the permanent 
successors are regarded by Stein as stigmata." 

Black 1 states that any malnutrition, even a burn, typhoid fever, 

1 Dental Review, 1906. 



MACROSCOPIC MALFORMATIONS 165 

a spasm, etc., may mark teeth as a nail may be grooved. He claims 
to have seen Hutchinson's teeth without history of taint. 1 

As it ordinarily causes embarrassment to question dental patients 
regarding syphilis, the Wassermann reaction may be resorted to 
if a diagnosis be needed. 

Stein states that the Wassermann may be positive or negative 
in heredosyphilis. 

The point at which the arrested development would occur, is that 
part under development at the time the nutritional or infective dis- 
turbance occurs. When several developing teeth are attacked, the 
centrals are marked nearer the neck than laterals, and these nearer 
than cuspids. The first molars are often occlusally defective, as well 
as incisors, and sometimes the incisors have only white or brown 
spots instead of the incisal notch; bicuspids are only rarely marked. 

Fig. 152 




Hutchinson's teeth, cuspal atrophy of canines and molars. Multiple sulciform erosions 

Diastema. (Cavallaro.) 

A lack of development of the anterior portion of the upper jaw 
has been noted in a number of cases clearly syphilitic (Fig. 147). 
It has been noted that not all syphilitic children present these dental 
appearances; and, again, appearances said to be identical with them 
are observed in children said not to be syphilitic; nevertheless, the 
presence of such teeth is usually regarded as a valuable diagnostic 
sign of hereditary syphilis. The existence of interstitial keratitis 
and of chronic catarrh of the middle ear, in connection with Hutchin- 
son's teeth are held to be positively diagnostic signs of hereditary 
syphilis (Hare). (See Sabouraud, p. 181.) 

Oberwarth, 2 in a synopsis of associate symptoms, mentions 
central deafness, chronic hydrarthrosis of the knee, periostitis of 

1 Dental Digest, 1904. 

2 Review by Dental Cosmos, 1908, p. 179. 



166 MALFORMATIONS AND ANOMALIES OF THE TEETH 

the tibia, tumefaction of the spleen and liver, radiating cicatrices of 
the lips, adenopathies, ozena, and deformities of the bridge of the 
nose, cutaneous gummata, hemoglobinuria, and cerebral phenomena 
as possibilities deduced from a study of his known cases of hereditary 
syphilis. • 

In 605 hereditary syphilitics observed by Sidler, Huguenin, and the 
Fourniers, the stigmata averaged as follows: ocular, 50 per cent.; 
dental, 43 per cent.; aural, 16 per cent. 1 

Therapeutics based upon such a diagnosis are followed by better 
results, as a rule, than when the general indication is ignored. The 
boy from whose mouth a model (Fig. 147) was obtained, had inter- 
stitial keratitis in the left eye, chronic nasal catarrh, and a somewhat 
flat development of the nasal bones. 

Tomes favors, and adduces evidence to support the contention of 
Hutchinson, that honeycombed incisal edges of incisors and cuspids 
and occlusal surfaces of first molars are indicative of mercurials 
administered in early childhood. 

Pitted, grooved, or otherwise malformed teeth may decay some- 
times so badly as to produce a black, slimy appearance almost 
loathsome to view. In other cases surprisingly little caries develops. 

Treatment. — If slightly pitted, silicate cement fillings are preferable. 
Single pits collect stains which are not removed by the brush. It is 
well to concave these with a small finishing bur, and to furnish the 
patient a sharply pointed stick, for cleansing with tooth powder or 
pumice. In some cases, grinding off the rough incisal edge is sufficient; 
in other cases the teeth may require to be drawn down after this 
procedure, or porcelain inlays may be used to restore the incisal 
edges. In the extremely disagreeable cases above mentioned, some 
form of crowning must be resorted to. Fig. 153 exhibits a restoration 
of the case shown in Fig. 145. For molars which tend to decay, 
amalgam or copper cements, white or black, are useful and when the 
cavities are broad or numerous a short gold crown may be fitted. 

Agenesia of Enamel. — Cases are observed where there has been a 
formative crisis to the extent of having apparently no enamel what- 
ever formed over the occlusal section of the crown, its deposit on 
the remainder of the crown being quite normal (Fig. 142). 

D. B. Freeman 2 records the case of an individual, aged twenty-six 
years, whose teeth anterior to the second molar were entirely devoid 
of enamel. The condition was hereditary; it appeared in both 
brothers and sisters, and could be traced back for three generations. 



1 Cavallaro: Dental Cosmos, 1909. 

2 Guilford: American System of Dentistry, vol. iii. 



MACROSCOPIC MALFORMATIONS 167 

Hopewell-Smith 1 claims that teeth apparently devoid of enamel 
have, in all cases examined by him, had attenuated enamel upon 
them. This would also be classified as hypoplasia. 

Black 2 has described the teeth of a man, aged twenty-seven years, 
as having enamel of an opaque, paper-white appearance, as readily 
cut as a slate pencil, and with dentin of ordinary consistence. The 
teeth presented little caries. He also described the temporary teeth 
of a child as all without trace of enamel, the dentin soft, bendable 
in any direction, with production of pain, and penetrable with a 
sharp explorer (agenesia of enamel). 

Hopewell Smith 3 has observed an entire absence of crowns, not 
due to wear or caries, both on upper and lower teeth, in four 
generations in one family. Therefore, they are cases of extreme 
hereditary agenesia of the crowns and are evidence of a possible tooth 
development independent of an enamel organ. 

Fig. 153 




Same as Fig. 145, with Land jacket crowns placed over anterior teeth. (W. A. Capon ) 

Anomalies of Development not of Dystrophic Character. — This 
subdivision will include all variations in size, form, number and 
development, clearly due rather to hereditary individual peculiarly of 
development or to accident rather than to nutritional or infective 
disturbance of developmental organs. 

Variations as to Size. — It is patent to the most casual observer 
that the teeth vary as to size. Comparisons in this direction are 
made by an examination of the upper central incisors. Fig. 154 
shows nearly the extremes of observable sizes; Guilford 4 points out 
that excessively large, central incisor crowns are usually supported 
by abnormally small conical roots. Marked giantism of the central 

1 Histology and Patho. Histology of the Teeth. 

2 Dental Cosmos, June, 1908. 

3 Ibid., August, 1913, p. 781. 

4 American System of Dentistry, vol. iii. 



168 MALFORMATIONS AND ANOMALIES OF THE TEETH 



incisors usually occurs in pairs, the other teeth being of normal size. 
On the other hand, dental giantism of less degree may involve all 
of the teeth of a denture. The molar teeth are occasionally of 
enormous size, the bicuspids rarely so, and the cuspids next in fre- 
quency to the molars as to the occurrence of giantism. Guilford 
observes that giantism of the cuspid crowns, unlike that of the 
central incisors, is usually accompanied by an increased size of root. 
He mentions the case of a cuspid measuring an inch and one-half 
in length from tip to tip. 

Fig. 154 





Dwarf Teeth. — Deficiency in size is of more common occurrence 
than excessive size. It appears to occur more frequently with the 
upper third molars and upper lateral incisors than with any other 
teeth. Fig. 155 shows the extremes in size between two perfectly 
formed lower third molars. The stunting of these and of other teeth 
is, however, usually associated with such an aberration of outward 
form that most dwarf teeth must be considered as abnormal in form 
as well as in size. The writer has seen a supernumerary with crown 
and root together measuring one-eighth inch. 

Fig. 155 




Tusk-like permanent central incisors; temporary teeth retained on either side. Female, 
aged twenty- five years. 



A central incisor, or more frequently a lateral incisor, may have 
a conical crown, as shown in Fig. 155. The condition may be double. 

Upper third molars frequently consist of but a single cone, diminu- 
tive in size; at times a crater-like crown is formed by a series of small 
cones about a central pit. 






MACROSCOPIC MALFORMATIONS 



169 



Treatment. — The Land jacket crown is very useful in modifying 
the cone into a typical tooth form (Fig. 156). 



Fig. 156 





Conical lateral incisor transformed by porcelain crown. 

Fusion of Teeth. — Two or more teeth may be united during the 
process of development. The union may occur (1) by the crowns, 
(2) by the roots alone, and (3) by both crowns and roots. 

1. Fused teeth united by the crowns alone have not been shown. 
The nearest approach to it is the case illustrated by Tomes, in which 
two central incisors have fused by union of the crown portions 
and one-fifth of the root portions of the two teeth (Fig. 157). 
Such teeth would have dentin common to both crowns at the point 
of union, the enamel being reflected over the outside of the common 

Fig. 157 





Lingual view. Labial view. 

Fusion of two permanent upper central incisors by their crowns and a portion of the 

roots. (Tomes.) 



dentinal mass, according to the scheme shown in the diagram Fig. 
161, B. The pulp may be common to the two teeth in the crown. 
Of course, the root pulps are separate. 

The condition is a record of the fact that prior to dentification the 
papillae and enamel organs of the two teeth have coalesced at some 
point. This must have occurred at an early period, perhaps even 
during the descent of the cords into the jaw. When it is considered 
that the two central incisors are contained in two separate inter- 
maxillary bones, the rarity of such a union and in such a manner 
may be appreciated. I have seen such a union between a right lower 



170 MALFORMATIONS AND ANOMALIES OF THE TEETH 

central and lateral incisor, in the mouth. Recession of the gum per- 
mitted a view of the cervical conformation. This case also disposes 
of the question raised as to whether fusion can pass the mesial line. 
Fig. 158 also shows a fusion of lower centrals. 

Fig. 158 




Fused centrals. (Batcheff, Dental Cosmos.) 

2. Those teeth united by fusion of the roots have a common dentin 
at the point of union, with cementum reflected over that. The pulp 
is common to the two teeth at the point of fusion. 

Fig. 159 




a b c d e 

a, fusion of two molars at the roots — two pulp cavities, one foramen; b, c, fusion of 
supernumerary teeth roots to buccal roots of upper molars, pulp canal common where 
probes cross; d, view of resorbed root end of two fusecl temporary teeth; e, concres- 
cence by hypercementosis. 



In the specimen shown in Fig. 159 at a there is but one apical 
foramen. In that shown at b and c there is but one foramen for the 
two fused portions of pulp, though the other canals have their usual 
foramina. These cases evidence an accidental coalescence of pulps 
after much independent root formation. 

3. Fusion throughout both crowns and roots have the same charac- 



MACROSCOPIC MALFORMATIONS 



171 




Fused denticles. 



teristics as the others, combined in the one specimen (Fig. 162). The 
diagram (Fig. 161) shows the scheme for the crown and root. 

Fig. 166 shows specimens of fusion in both the 
upper and lower jaws. It occurs also with the 
temporary teeth (Fig. 167). Fig. 160, A shows a 
very rare condition, the fusion of the temporary 
central, lateral, and cuspid of one side (triple fusion). 
Fusion is evidently an abnormality of develop- 
ment, dependent upon coalescence of formative 
organs at some point, and is most likely to occur 
where the adjacent tooth follicles have least anatom- 
ical separation from their fellows. The roots of fused temporary 
teeth are resorbed as usual (Fig. 159, d). 

No particular treatment is re- 
quired unless the mass in some 
way causes interference with func- 
tion, which is unusual. The teeth 
having a common pulp, no attempt 
should be made to divide them. 



Fig. 162 



Fig. 161 





A, diagram of a case of triple fusion, 
showing crowns with independent in- 
cisal edges and pulps; but otherwise 
fused into one crown with one pulp; 
B, transverse section of same, showing 
common pulp cavity and common den- 
tin overlaid by enamel (or cementum). 
From a perfect specimen in the editor's 
collection. (Enlarged.) 




Permanent central and lateral incisors of 
the upper jaw, united throughout the whole 
length of the teeth. (Tomes.) 



Fusions are most common between the anterior teeth of each set and 
between the second and third, or third and fourth (supernumerary), 
permanent molars. It has rarely been noted in bicuspids, presumably 
because these teeth lie in the bifurcations of the temporary molars, 
but Fig. 163 shows a case of fusion of a bicuspid and molar, the 
only one ever brought to the writer's attention. 

Concrescence of Teeth. — Concrescence of teeth is their union after 
the tooth is formed; it is evident, therefore, that the union can only 
be caused by fusion of cementum. This means that during the 
formative and eruptive period, or after eruption, the bony partition 
between the teeth disappears, and that their pericementi become 



172 MALFORMATIONS AND ANOMALIES OF THE TEETH 

united, receding from the line of compression as cementum is 
deposited between and joining the roots. The united teeth show 
evidences of hypercementosis at points other than the point of union 
(Fig. 159, e, and Fig. 169). At times the roots of the' same tooth 
undergo either fusion or concrescence. 





Fig. 163 




1 ^P 






^K ; 







Fused bicuspid and molar. 



Fig. 164 



During the eruption of the third molars, particularly the upper, 
temporary lack of space for the eruption of the crown may cause 
resorption of the bone covering the roots of the second molar, and 
fusion of the formative pericementum of the third molar with that 
of the second occurs; a deposition of cementum then binds the teeth 
together, preventing the eruption of the third molar. More than 
two teeth may be thus united. The lower third molar rarely pre- 
sents its roots to those of the second molar; the 
contrary presentation is the rule. 

In at least one case, the crown of the upper 
third molar was partly erupted when concres- 
cence occurred. Retained in this situation, the 
crown decayed away, necessitating extraction; 
the second molar came away with it. The 
condition also occurs apart from the eruptive 
process. Excessive hypercementosis upon the 
roots of individual teeth may finally result in 
their union (Fig. 159, e). 
The only treatment required for concrescence is that indicated 
for impaction or hypercementosis (which see). 

The tough fibrous gum tissue or pericementum has caused two 
temporary teeth to be extracted together at times (Fig. 168). 

Pont cites a case of attachment of a lower first molar distal root 
to the mesial root of the second molar by a strong fibrous ligament, 
2 mm. in diameter, and causing fracture and removal with the first 
molar. There is also sometimes a firm fibrous pericemental attach- 




Fusion of a super- 
numerary tooth, with 
an upper third molar. 






MACROSCOPIC MALFORMATIONS 



173 



ment between a tooth and the alveolar process or bone. In one 
case a portion of the antral floor was torn out with the apical tissue. 



Fig. 165 




Geminous upper laterals with common pulp. Practice of Dr. Varney Barnes. 
(Radiograph by E. Ballard Lodge.) 

Fig. 170 illustrates a remarkable case of combined fusion, 
concrescence, flexion, and hypercementosis. In this case two 
abnormal third molar crowns were first formed. The roots were 
fused during development, though individual single-pulp canals 
were formed, which joined to form one foramen. The lapped condition 

Fig. 166 




A, fusion of upper geminous, permanent laterals; B, fusion of lower right permanent 
central and lateral incisions. 



of the roots was due to pulp flexion previous to root deposition. The 
carious second molar roots all became hypercementosed and probably 



174 MALFORMATIONS AND ANOMALIES OF THE TEETH 

from non-occlusion, or the widespread irritation aroused by the fused 
teeth in descent. As the fused teeth erupted, they presented one 
root to one root of the second molar. 

Fig. 167 




Fusion of upper temporary teeth. Double fusion of lower temporary lateral and 

cuspid. 



Fig. 168 



Fig. 170 




Attachment of temporary teeth by their 
pericemetin. 



Fig. 169 





Concrescence. Third upper molar imprisoned 
between the roots of the second molar. 



Case of fusion of two abnormal 
molars and concrescence with the 
root of a right upper second molar 
(restored for illustration.) Pulp 
canals shown in outline. Common 
apical foramen (enlarged.) (From 
author's collection.) 



II 



MACROSCOPIC MALFORMATIONS 175 

The junction of these occurred as the result of formations of cementum 
(concrescence) . The widely open crater-like pit in each crown shows 
the persistence of soft tissue (enamel organ) at that point, and a 
lack of enamel development there. 

Mechanical Union of Teeth. — Teeth upon extraction are occasion- 
ally found united by alveolar bone which is locked between the 
roots of the two or more teeth and prefers to fracture elsewhere. 
Occasionally a sequestrum contains several teeth (Fig. 72). 




Double gemination of upper permanent lateral incisors. 

Gemination of Teeth (Twin Teeth) . — This term has been used by 
Tomes in the sense of union of teeth, but it is perhaps better used 
to designate supplemental teeth of the same class. In twin teeth, 
the enamel organ of a permanent or temporary tooth is duplicated, 
in all probability, two buds arising from the cord or band, as the 
case may be. 

In gemination, one of the teeth formed is, of course, a supernu- 
merary tooth, but in some cases both are typical teeth (Fig. 171). 
The second germ may develop an atypical tooth or one but slightly 
abnormal in form. The geminous teeth may undergo fusion, as seen 
in Figs. 165 and 166, A. 

Duplication of the Pulp Cavity. — Hopewell-Smith calls attention 
to a case of an upper permanent central incisor containing two pulp 
cavities in the coronal portion, probably an interrupted gemination. 

Tooth Inclusion. — Dens in Dente. These terms refer to the inclu- 
sion of one tooth^within another. 

Cohen 1 attributes the first description of the anomaly to Busch 

i Dental Cosmos, March, 1919. 



176 MALFORMATIONS AND ANOMALIES OF THE TEETH 

and seems to regard it with him as one tooth structure built circu- 
larly around another. The peculiarity noted is that the primary 
tooth has a root with cementum outside and dentin inside while the 
dens in dente has cementum inside and dentin outside. He offers 
some illustrations which are particularly interesting as showing the 
enamel-covered crown of a supernumerary tooth penetrating the 
unfinished apical foramen of the primary tooth. 



Fig. 172 



Fig. 173 




1 ^El 


f 




Kirk, Dens in Dente. 



Lingual and buccal half of the matured dens in 
dente. (Cohen.) 



Kirk, 1 in describing the anomaly shown in Fig. 172, theorizes 
" that it arose from an invagination of a portion of the dental follicle 
including some portion of the enamel organ on the same principle 
that dermoid cysts arise from invagination and inclusion of portions 
of blastoderm within the body of the organism." 

Inasmuch as the descent of supernumeraries formed outside of 
teeth upon teeth in the mouth is known and their occasional pro- 
duction of resorption of permanent roots by such descent is known 

1 Dental Cosmos, June, 1918. 



MACROSCOPIC MALFORMATIONS 111 

and Cohen illustrates one at the root apex apparently entering it and 
Fig. 172 shows one completely formed and lying to all intents free 
in the pulp cavity and surrounded by space for pulp tissue, the 
writer is inclined to believe that a supernumerary has descended 
squarely upon the open foramen of an undeveloped primary or pre- 
ceding tooth and has penetrated the wide pulp tissue causing it to 
bulge upon the sides and around it. In the case in Fig. 172 this 
must have occurred early in root development of the primary tooth 
at, say nine years of age. 

The surrounding pulp and its outer follicle wall then formed a very 
large root which went on to almost completion. 

To account for the dentin outside cementum inside of the root of 
the secondary tooth we may theorize that its crown pushed down the 
follicle wall normally around all formative pulps (papilla), so that 
the secondary tooth was surrounded by a soft tissue arranged thus: 
follicle wall inside, pulp tissue outside. The calcification would then 
be as claimed by Cohen, though the pulp of the supernumerary is 
not thus taken into account. Even in odontomes the calcific forma- 
tions are held to result from the respective formative tissues and 
while the pulp of the secondary tooth might possibly form cement- 
like structure under irritation (see Pulpitis), it is probable the follicle 
wall and pulp in some manner became arranged as suggested. It 
would be interesting to know if Kirk's tooth had this histological 
arrangement. 

Harrower's case (Fig. 49) shows a tooth inclusion due to explain- 
able forces, i. e., a pushing up of the permanent crown into the pulp 
of the temporary tooth which in turn has become an absorbent organ 
and hollowed out the temporary crown. Again Fig. 172 shows what 
looks much like secondary formation just below the tip of the super- 
numerary crown which is evidence of interference with pulp function. 
Raper illustrates a radiograph of a similar anomaly from the practice 
of Dr. Van Woert. 

The formation of so much root as Cohen's case shows before the 
supernumerary is included seems to prove that the inclusion is acci- 
dental and not a heterogeneous arrangement of germs or tissues. 

Dilaceration. — By dilaceration is meant a displacement of a formed 
portion of a tooth in such a manner as to change its relative position 
to the soft parts engaged in its development, the development then 
being continued in the new relation. 1 For example, an accident to 
a temporary tooth occurs and the force may displace the partially 
formed permanent crown, altering its relation to the enamel organ 

1 Tomes. 
12 



178 MALFORMATIONS AND ANOMALIES OF THE TEETH 

and papilla engaged in its formation. The balance of the crown 
may be formed in the new situation and be of fairly perfect or of 
imperfect structure (Fig. 174). This is most likely to occur with 
the anterior teeth, especially when a temporary tooth is driven into 
the alveolar process, its root in turn displacing the permanent tooth, 
thus twisting its relation to its formative organs. I have a beautiful 
specimen of a fossilized tooth from a Florida Indian mound showing 
this condition. 1 



Fig. 174 





BofR 



Pulp hernia and flexion, mesiodistal 
section: E, enamel, distal section in the 
bifurcation of the roots, flexion of enamel 
organ; D, dentin; C, C", cementum; PC, 
pulp cavity, flexion of pulp with hernia or 
at least abnormal enlargement before root 
formation; F, large apical foramen; B of 
R, bifurcation of the roots. (From a speci- 
men, enlarged.) The whole is a radicular 
odontoma. 

Fig. 176 



Dilaceration. Shows fold in the labial 
enamel and cervical dentin. (After von 
Wunschheim. 2 ) 




Enamel excrescences. (Salter.) 



Flexion. — Flexion means the movement of one of the formative 
organs of a tooth away from its normal relation to the hard part it 
is developing. The soft part has its position altered, the hard part 
remaining in correct position. Subsequent formations therefore 
have an abnormal relation to the previously formed portions of the 
tooth. 



1 Kindly presented by Dr. Simpson, of Kissimee. 

2 G. von Wunschheim: Fracturen. Infraktionen und Knickungen der Zahne. 



MACROSCOPIC MALFORMATIONS 



179 



As an example of flexion, a portion of the enamel organ of a tooth 
may be displaced and in its new relations may form enamel in an 
unusual situation, as, for example, upon the side or neck of the root 
(see enamel nodule) or even in the bifurcation or on the apex of the 
root (Figs. 175 and 178). Again, it is probable that lack of space 
may cause deflection of a pulp engaged in root formation, a curved 
root being the result (Fig. 184). The pericementum (follicle wall) 
moves with the pulp in these cases. 

Unusual Locations of Enamel. — That during development, the enamel 
organ or portions of it, may assume an abnormal relation to the pulp, 
is evidenced by odontomes. Apart from these, there are evidences 
seen in teeth which show that portions of the enamel organ may 
become detached from the main organ, and develop enamel in unusual 
situations. Thus columns of enamel may penetrate the body of the 
dentin, i. e., the enamel organ has lain within the papilla. 



Fig. 177 



Fig. 178 





Lower molar with enamel nodule 
connected to the enamel of crown by 
a ridge of enamel. 



Five-rooted upper molar, cap of enamel 
on end of one root. Possibly a fusion of 
a supernumerary. 



A small nodule or cap of enamel overlying dentin, and itself over- 
lapped at the edges by cementum (Fig. 179), may be found upon the 
root of a molar, usually upon the side of an upper third molar at a 
point about one-eighth inch from the cervical margin of the crown 
enamel; but one may be one-half inch distant from the enamel mar- 
gin. A thin ridge of enamel sometimes, though not usually, seen 
connecting them, indicates the nodule to have been formed by a 
detached portion of the original enamel organ (Fig. 177). This forma- 
tion is known as an enamel nodule. It may occur upon a lower 
molar, though usually found upon the upper molars. Two may 
exist on opposite sides of a molar, as in a specimen possessed by the 
editor. They may cause neuralgia. (Ottofy.) 

A molar root may have a cap of enamel upon its apex, an evidence 
of extreme displacement, even more than shown in Fig. 178. Some- 



ISO MALFORMATIONS AND ANOMALIES OF THE TEETH 

times an enamel ridge runs down the side of a root; sometimes an 
excrescence may be found upon the enamel (Fig. 176). Fig. 175 

Fig. 179 




Structure of enamel nodule. E, enamel; D, D, dentin. (Hopewell-Smith.) 

shows enamel formed in the bifurcation of the roots of a lower 
molar. The enamel nodule has been explained upon the hypothesis 



Fig. 180 



Fig. 181 



Fig. 182 




Upper molar 
with supplemental 
cusp on lingual 
side. 




Showing talon-like un- 
usual development of 
the cingule on an incisor. 
(From case reported by 
W. H. Mitchell, Dental 
Cosmos, vol. xxxiv.) 






Very large supplemental cusp 
on the buccal surface of upper 
molar. Probably a fused "para- 
molar." 



that the remains of the epithelial root sheath of Hertwig have within 
them the inherent power of forming enamel, which may account 
for enamel on the side or end of a root. As this epithelial root-sheath 



MACROSCOPIC MALFORMATIONS 



181 



is probably the trailing remains of the enamel organ left as the 
organ is carried up by the tooth, it is quite likely that larger portions 
of the organ may be detached as above explained. (See Fig. 186.) 



Fig. 183 



Fig. 184 



Fig. 185 





Cuspids with long roots. 



Curved roots. Upper cuspid with two roots. 




Supplemental Cusps. — Occasionally a tooth has a greater number of 
cusps than usual. The most common form of this condition is a 
supplemental mass attached to the palatal side of the mesopalatine 



Fig. 186 




Developing tooth showing Nasmyth's membrane over enamel; also, Hertwig's root 
sheath. (Section by Addison.) 

cone of the upper first molars (Fig. 180). Sabouraud 1 claims that 
this is a sign of syphilis even when occurring as the only stigma in 
an otherwise perfect set of teeth and claims twenty consecutive 

1 Dental Cosmos, 1917, pp. 759 and 1043. 



1S2 MALFORMATIONS AND ANOMALIES OF THE TEETH 

positive Wassermanns in connection with it. Mozer and Chenet 
found but one such cuspal arrangement among sixty children known 
to be syphilitic, and among those in whom no taint was discoverable 
the cusp was found nineteen times. Twenty-three men examined by 



Fig. 187 



Fig. 188 



Fig. 189 






Short buccal root of a 
molar, otherwise properly 
developed. 



Central incisor with 
short root. 



Five-rooted upper third 
molar. 



Jeanselme 1 having this cusp gave negative Wassermann tests. It 
would therefore seem not pathognomonic but might be used as a 
point of suspicion if a lesion of unknown origin exists and the 
patient be subjected to the Wassermann as Sabouraud has claimed 
advantage in several cases. It is more rarely the 
case that a cingule of this sort is noted upon the 
lower molars. The palatal tubercle, the promi- 
nence upon the cingule of an upper incisor, may 
be of exaggerated size. In one case (Fig. 181) 
this development gave the appearance of a talon 
upon the tooth, a distinct cusp segment in itself. 
Fig. 182 illustrates a marked supplemental cusp 
upon the buccal surface of a molar. A fusion in 
this location is not impossible. (See Fourth 
Molar.) 

Malformations of Roots. — Differences in regard 

to the size, arrangement, form, and number of 

the roots of teeth are the most common of the 

dental malformations. The roots of teeth may be 

abnormally long (Fig. 183) or abnormally short 

(Figs. 187 and 188). 

The roots of cuspids may be bifurcated, particularly in the lower 

jaw (Fig. 185). A central may have a short supplemental root. 

(Guilford 3 ), or sometimes two distinct roots as in Fig. 190. 




Two-rooted upper 
right central incisor 
(Warren. 2 ) 



1 Dental Cosmos, 1918, p. 447. 
3 American System of Dentistry. 



2 Dental Brief, April, 1913. 



MACROSCOPIC MALFORMATIONS 



183 



The upper first bicuspids may have trif urcated roots, the extra root 
usually being on the buccal aspect. The upper second bicuspid may 
be bifurcated; upper molars may have more than three roots, the 



Fig. 191 



Fig. 192 



Fig. 193 






Two-rooted lower cuspid. 
Resorption of temporary 
roots. (Radiograph by E. 
Ballard Lodge.) 



Fibrous odontome. 
(Garretson, after 
Pierce.) 



Results of hernia of 
pulp. (Salter.) 



Fig. 194 




Fig. 193 magnified. 



1S4 MALFORMATIONS AND ANOMALIES OF THE TEETH 

third molar often having four, five, or six, and in one case reported, 
eight roots (Figs. 178 and 189). In some cases upper third molars 
have but one root with a single, large canal, a case of true develop- 
mental fusion or, so to speak, original intent of the pulp which has 
not divided as usual. In other cases the roots are fused so as to form 
apparently but one root, while the canal divisions may exist. This 
may be fusion or concrescence of roots. Lower molars may have 
three or four distinct roots, but rarely only one. 

Abnormalities of root form are of extreme frequency, and are 
probably explained upon the hypothesis of flexion of the root pulp, 
previous to the deposition of the curved portion of root tissue. 

It is impossible to diagnose the forms of roots from the appear- 
ance of the crowns, but a skiagraph will determine their form with 
certainty. It may be said, however, that narrow necks indicate a 
probable divergence of roots, and vice versa. 

An excrescence upon the cementum is known as a cemental nodule. 



Fig. 195 



Fig. 196 




Radicular odontome. (Tomes.) 




Odontoma. (Garretson.) 



Odontomata. — An odontoma is a growth composed of structures of 
which the teeth are composed, but the masses may be so arranged 
as to have no typical form or even resemblance to a tooth. They may 
appear in the arch or may remain embedded in the jaw, where they 
may lie quiescent or may excite cyst formation (Fig. 82, page 187), 
or give rise to various morbid reactions, such as tumor formation. 

It has been held by Broca that any of the formative organs of the 
tooth — enamel organ, dentinal papilla, or follicle wall — may undergo 
aberrant development and may thereafter deposit calcific tissue or 
not, as the case may be. If not, soft tumors of the jaw, not dis- 
tinctly dental, may form, though in its complete form such a tumor 
may become a seat of calcific deposition peculiar to the aberrant 
tissue. 

Bland-Sutton's classification is usually adopted, and is as follows: 

1. Aberrations of the enamel organ: (a) Epithelial odontomes. 
(b) Calcified epithelial odontomes. 



MACROSCOPIC MALFORMATIONS 185 

2. Aberrations of the follicle: (a) Follicular cysts, (b) Fibrous 
odontomes. (c) Cementomata. (d) Compound follicular odontomes. 

3. Aberrations of the papilla : (a) Radicular odontomes. (6) Den- 
tomata. (c) Osteodentomata. (d) Cementomata. 

4. Aberrations of the whole tooth germ (or three formative 
organs), composite odontomes. 

The Uncalcified Odontomata: 1. Epithelial odontomata which 
arise by aberrant development of the enamel organ, and remaining 
uncalcified resemble the adenomata. 

2. Follicular odontomata: (a) The wall of the follicle is distended 
and the cavity is filled with a thick fluid (sometimes pus if infected), 
and contains a portion of imperfectly developed tooth. It is in this 
form really a cyst (Fig. 82). It is probable that the enlargement 
is due to the aberrant development of epithelium existing in the 
pericementum as the root sheath of Hartwig (pericemental glands 
of Black). After a mass is formed, degeneration of the central part 
into a liquid forms a cavity, lined with epithelium and contain- 
ing fluid. The cyst formed in so-called granuloma at the end 
of roots containing dead pulps may come under the classification of 
follicular cysts, as it conforms at times to the above description and 
the pericementum is really a remains of the follicle wall. (6) The 
follicle wall or pericementum may thicken so as to form a fibrous 
capsule about the tooth, sufficiently resistant to prevent its eruption 
(Fig. 192). This is called a fibrous odontome and is considered rare. 

3. Compound follicular odontomata: The follicle wall thickens 
into a fibrous capsule, and in this may appear fragments of cemen- 
tum, dentin, or imperfectly formed teeth with their enamel, dentin, 
and cementum. 

It is a combination of an uncalcified and calcified form, and might 
easily lead to formation of a cyst containing many teeth or portions 
of teeth (a dentigerous cyst, Fig. 82). 

The Calcified Odontomata: 1. Epithelial. The enamel organ 
develops aberrantly into a large, possibly multilocular mass, and 
enamel deposition occurs, forming a large mass composed of enamel. 
The enamel nodule, while much simpler and of fairly obvious origin, 
is now classified as odontomatous. 

2. The Cementomata: A fibrous odontome forms from the follicle 
wall, then calcifies into laminated ossific material. One from a 
horse, in the Royal Veterinary College, London, weighed seventy 
ounces. It may include one or more teeth. 

3. Radicular Odontomata: The crown may form normally, but 
the dentinal papilla becomes aberrant and develops largely, conveying 
with it the follicle wall. Ceasing to enlarge, cementum and dentin 



1S6 MALFORMATIONS AND ANOMALIES OF THE TEETH 

are deposited somewhat in the ordinary manner, but of somewhat 
aberrant deposition. Pulp hernia comes under this heading and 
acts similarly (Figs. 193 and 195). 

Fig. 197 




Composite odontome. (Garretson.) 
Fig. 198 




Composite odontome. (Garretson.) 



4. Composite Odontomata: The developmental organs, the 
enamel organ, the papilla, and follicle wall are aberrant, hetero- 
geneously arranged, enlarged, and then deposit a composite mass, 



MACROSCOPIC MALFORMATIONS 



187 



which may be somewhat orderly and tooth-like (Fig. 196), or be 
totally unlike a tooth as in Fig. 198. 1 

The diagnosis of odontoma, if at all obscure may be made by 
radiography (Fig. 200). 

Treatment. — The treatment of odontomata is usually that directed 
to their sequels, which consist of enlargements about the jaws with 
more or less inflammation or cyst formation, and, as a rule, involves 
their removal by surgical operation. 

Fig. 199 




Structure of a composite odontome. (Garretson.) 

Cysts. — A cyst is an enlargement containing a cavity, which, 
in turn contains liquid, gelatinous or pultaceous, material, about 
which is a capsule condensed from the surrounding structures. 
The accumulation of the fluid or semifluid contents produces the 
enlargement of the part even if bony (Fig. 82). 

They differ from tumors in being strictly localized, though they 
may be large, and in their generally benign character, though tumors 
may at times have a cystic character. 

Cysts may be formed by the retention, secretion, or extravasation 
of fluid in several ways: (1) By the retention of normal secretion of 
a gland owing to the obstruction of its duct — e. g., ranula. These 
are called retention cysts. (2) By abnormal secretion into ductless 



1 The classification of odontomata by Bland-Sutton has recently been modified 
by the British Dental Association, but does not seem to the writer to offer definite 
reason for substitutions. For a synopsis, see Dental Cosmos, February, 1916, p. 227. 



188 MALFORMATIONS AND ANOMALIES OF THE TEETH 

cavities — e. g., bursas (exudation cysts). (3) By the extravasation 
of blood into a ductless cavity (extravasation cyst). (4) Indepen- 
dently in tissue as a result of mucoid or fatty changes or liquefaction 
necrosis, the surrounding tissue becoming condensed into a capsule 
(liquefaction or colliquation cysts). (5) Independently as a collection 
of fluid in connective-tissue spaces, which enlarge and fill. The 
surrounding tissue condenses into a cyst wall. (6) Independently as 

Fig. 200 



^^^w ^H a resu lt °f chronic irritation by 

J ^H^^^H foreign bodies, extra vasated blood, 

^^^^■ri^^^^^^^H or parasites, as in dentigerous 

■|HHH^^^^H cysts 1 (Fig. 82). Cysts may have 

but one cavity (simple cysts) or 
Surgical fracture of mandible, with have numerous intercommunica- 

photograph of odontoma and molar . ... , i i- / 

tooth after removal. (Graham.) tin g Cavities known as locull (com- 

pound or multilocular cysts). 
Forming within bony walls, these may be largely distended, and the 
walls are usually thin. There is generally a crackling sound produced 
upon pressure. Dentigerous and other cysts are usually lined by epithe- 
lium peculiar to the part. The explanation of Malassez, that epithe- 
lial remnants (of the enamel organs) develop, forcing the connective- 

1 Green: Pathology and Morbid Anatomy. 



MACROSCOPIC MALFORMATIONS 189 

tissue elements outward as a covering to them, is probably the correct 
one. Meanwhile, fatty degeneration of developed epithelium and 
the collection of fluid account for the fluid or pultaceous character 
of the cyst contents. This proliferation of epithelial remnants is 
well proved by the development of epithelial products in the interior 
of dermoid cysts. (See Fig. 203.) 

Fig. 201 




Longitudinal section of a tooth from an ovarian cyst: a, b, d, tissue filling absorp- 
tion cavities; c, narrow band of connective tissue through which the organ a received 
its nourishment; d, absorption of enamel. (Miller.) 

Dermoid cysts are cystic tumors of widely varying sizes found in 
various parts, such as the ovary, neck, base of brain, orbit, etc. 
They contain fatty and epithelial debris, and are lined with epithe- 
lium, outside of which is a corium with its papillae, and outside of 
this subcutaneous adipose tissue. The whole is inclosed in a fibrous 
capsule of connective tissue. The epithelial lining may contain 
and develop the characteristically dermoid structures, hair, teeth, 
sebaceous and sweat glands (Fig. 203). 

Broomell 1 states that the hair is often several feet long, usually 
of a light brown color, regardless of the color on the outside of the 

1 Dental Cosmos, 1905. 



190 MALFORMATIONS AND ANOMALIES OF THE TEETH 

body, and becomes white as age whitens the outside hair, and is 
usually absent in dermoids in bald persons. Hair follicles are present. 
He states : " Dermoids of the mouth are usually found in the hard 
and soft palates, infrequently in the former, but when found are 
complicated, while the more frequently found in the soft palate 
are simpler. In these situations they range from the size of a pea 
to that of a hen's egg, the larger being pendulous. They are also 
found on the floor of the mouth and dorsum of the tongue. Brown 
instances a case in which one lay under the jaw and extended down 
the side of the neck. 1 Blair 2 states that when not found in such 
a situation they occupy a position beneath the skin between the 
geniohyoglossi muscles. 

Fig. 202 




Absorption tissue, from cavity a in Fig. 201. 



"The teeth range in shape from the simple cone to multicusped 
complex forms, the crowns of the same being well formed. The 
roots are usually not fully calcified or developed, or, perhaps, partly 
developed. A follicular wall is present. The enamel may be smooth 
or pitted. 

"The cementum is usually absent or but slightly developed. 

1 Dental Cosmos, 1908. 

2 Surgery and Diseases of the Mouth and Jaws. 



MACROSCOPIC MALFORMATIONS 191 

"Radicular odontomes evidenced by tumor-like growths on roots 
are due to aberration of the dentinal germ. The pulp canal was 
always present in cases examined. Fusion of teeth has occurred in 
these cysts. In histology the teeth are similar to ordinary teeth, 
with some slight aberration due to the peculiar condition." 

According to Eccles and Hopewell-Smith, 1 the teeth may be found 
imbedded in alveoli in bone; that a small jaw with normal-sized 
teeth may exist. 

Miller 2 states that the cystic contents include fatty acid, oxalic 
acid, large quantities of tyrosin and leucin, which substances furnish 
the acid for the decalcification of teeth occasionally found, but that 

Fig. 203 




Portion of a wall of an ovarian dermoid cyst: a, wall of the cyst; b, projecting portion 
made up of fatty and cutaneous tissue; c, hairs; d, teeth. (Ziegler.) 

no bacterial action, such as occurs in the second stage of dental 
caries, could be found. He stated that in those teeth having living 
pulps transparency might be found. 

Tumors. — A tumor is a swelling. The term therefore includes all 
benign enlargements as well. Garretson divided them into: 

1. Those having an explanation in local conditions which are 
cured, upon correction by surgical means. 

2. Those unexplainable upon such ground (ordinarily termed 
neoplasms). These are due to abnormal cell growths incited by 
causes not clear, cause swelling and sap vitality and if of malignant 

1 Proceedings of the Royal Society of Medicine. 

2 Dental Cosmos, 1905. 



192 MALFORMATIONS AND ANOMALIES OF THE TEETH 

variety, eventually cause death by toxemia or metastasis. The 
consideration of tumors belongs to "oral surgery." A tumor is 
obvious and if not of the first class should be referred to a surgeon 
for diagnosis and treatment. 

Occasionally a benign growth arises from the gum which fills 
with blood upon circulatory excitement (epulo-erectile tumor analo- 
gous to a nevus) or a small growth may begin about a tooth socket. 
Sarcoma which if not apparently due to conditions about the teeth 
and not subsiding as an inflammatory tissue should be referred to a 
surgeon for examination. A small piece may be taken for histo- 
logical examination. Upon the hard palate or along the jaws a 
bony protuberance, otherwise healthy looking, known as an osteoma 
may be seen. The patient occasionally does not know of it. It 
is benign. A small rounded excrescence is occasionally seen upon 
the cheek or lips. It seems long-continued and benign but should be 
referred for examination. Ulcers upon the tongue should be considered 
in the light of syphilis or epithelioma. A small papilloma may be seen 
on the tongue. Leukoplakia frequently seen should be thought of in 
connection with syphilis and carcinoma. (See Index.) Cases of grave 
tumors of the jaws are frequently seen in oral clinics which are the 
cullings of a large community or district. They are rarely seen in 
dental practice, but one should be on the lookout for the above slight 
conditions and refer them to oral surgeons. 

Anomalies of Number. — Although the dental series of man nor- 
mally consists of thirty-two members, cases are frequently observed 
in which the number is less than, or in excess of that number, or there 
is an abnormal number in any particular group of teeth. 

Deficiency. — It is observed with some frequency, that the upper 
lateral incisors never make their appearance, a condition traceable to 
the influence of heredity in some of the instances. In an interesting 
case of three sisters, who all were without upper laterals, a son of one 
of them had them. Unfortunately the history, as to the parents of 
the sisters, was not certain, as they wore artificial teeth. 

When the laterals are absent, the permanent cuspid erupts and 
occupies the lateral incisor space, and thus sometimes fails to cause 
resorption of the root of the temporary cuspid, which persists in the 
cuspid space (Fig. 52). The lower laterals sometimes, but more 
rarely, fail to appear; are probably never formed (Fig. 204). The 
third molar may never appear, or appear as a peg-like tooth. Usu- 
ally the diminutive tooth is in the upper jaw but rarely it appears 
in the lower. These appearances are confirmed by reports of radiog- 
raphers. 1 

1 Johnson's Operative Dentistry. 



MACROSCOPIC MALFORMATIONS 



193 



The cuspid often is impacted but is seldom lacking in formation. 
Usually when missing it is to be found by radiography but may be 
absent. Kells reports such a case. I have recently had a lajly 
patient, sixty-four years of age, with a temporary lateral and 
cuspid loosening. Radiograph shows a cuspid descending. 

The cases of suppressed teeth, next in point of frequency, are 
those of the bicuspid teeth. If the corresponding teeth are all 
present in the dental arch, a well-founded suspicion of impac- 
tion of the missing tooth may be entertained and a radiograph 
resorted to. 

Fig. 204 




Absence of both upper and lower laterals in the same mouth. Temporary left upper 

cuspid. 



An excessive growth of hair upon the face and body has also been 
associated, in some cases, with a deficiency in number and altera- 
tion in form of the teeth. In other cases no abnormality was notice- 
able. 1 In some cases the hair and other dermal structures may be 
normal and the teeth be quite deficient in number. 

The extreme of suppressed formation is represented in a case 
described by Guilford. 2 

A patient over fifty years old had never erupted any teeth, tem- 
porary or permanent; the alveolar arches revealed no evidences of 
enclosed teeth, but had the appearance of typical edentulous jaws; 
the alveolar bone itself was but primitive. The case appeared to be 
sporadically hereditary, a grandparent and an uncle exhibiting a 



1 Tomes: Dental Surgery. 
13 



American System of Dentistry, vol. iii. 



194 MALFORMATIONS AND ANOMALIES OF THE TEETH 

like condition. The cases are interesting also because of additional 
evidences of faulty evolution of dermoid structures. In the first 
case cited, no sudoriparous glands appear to have formed, and there 
was but a faint growth of hair on the cranium, and none on the 
face and body. The uncle was hairless and edentulous from birth. 
Guilford found, in other members of the family, an absence of the 
full complement of teeth. 

Gibbs 1 reports two brothers, respectively six and a half and seven 
and a half, as without teeth or sweat-glands. It appeared to be 
an accentuation of atavistic heredity on the mother's side. 

In an interesting summary, Kjaer 2 quotes Trueswell as knowing 
of a man, aged fifty-four years, having had no permanent teeth, but 
all of his temporary ones, and Fricke as having 3 cases of retention 
of temporary teeth until sixteen, eighteen, and twenty years respec- 
tively, when the permanent teeth appeared, and Linderer as having 
a case of a lady, aged sixty years, who never had any teeth, and a 
case of his own in which the temporary teeth were lost from time to 
time, but no permanent successors appeared, and none could be 
detected by radiography. He attributed the lack to some disturb- 
ance during fetal life, as the family history did not include such a 
case. 

Excess. — The possible occurrence of a condition in some respects 
the reverse of the preceding, has been much written of and discussed 
— i. e., the occurrence of a complete third denture. There can be but 
one conclusion from an examination of all the evidence thus far 
presented, and that is that no clear and well-authenticated cases are 
made out. Isolated cases of the appearance of teeth subsequent to 
the loss of all of the second denture are not infrequent; and, so far 
as clear records can be obtained, are resolvable into cases of the 
eruption of supernumerary or impacted teeth, though sometimes 
a number of teeth are reported erupted. While these cases are, 
at least for the present, to be held as unproved in connection with 
elderly persons, a well-authenticated case of multiple dentition in 
a child is recorded by Catching. 3 Between the sixth and seventh 
month the eruption of one set of teeth was complete; within three 
months all of these had been lost. Between the eleventh and fifteenth 
months another period of dentition occurred, the teeth of this second 
denture being of such faulty structure as to crumble away quickly. 
At the age of two and one-half years a third dentition appeared, 
which caused the child such inconvenience that the teeth were 

1 Dental Cosmos, March, 1916, from Dental Record, London, November, 1915. 

2 Dental Cosmos, 1907. 

3 Southern Dental Journal, October, 1886. 



MACROSCOPIC MALFORMATIONS 195 

extracted by the mother. At the age of eleven years a fourth series 
erupted, incomplete through the absence of six teeth. At the age of 
fifteen years these teeth were sound and firm. 

The Fourth Molar. — Very rarely a fully developed fourth molar 
appears in the maxilla. In one case it was impossible to distinguish 
the normal. The third and fourth lay in lingual and buccal relation. 
Less rarely, a less typical molar appears posterior to the third molar. 
This must be very rare in lower molars. A third type of super- 
numerary appears in the maxilla. These are rudimentary, and 
appear upon the buccal side, opposite the approximation of the 
first and second molars or of the second and third molars, or to the 
distal or distolingual of the third molars. Bolk 1 calls the buccal 

Fig. 205 




The fourth molar. In situation usually occupied by a paramolar. (Hartman.) 

supernumerary the "paramolars," and says they are small, two- 
cusped, single rooted, and, if fused, usually unite with the mesio- 
buccal portion of the tooth posterior to it during development. Here 
it forms a supplemental section, "paramolar tubercle" (Fig. 206), 
which may have a distinct " paramolar root" or root indication. Bolk 
accounts for the less frequent appearance of an anterior independent 
paramolar (opposite the approximation of the first and second molars) 
upon the supposition of a more frequent fusion with the second molar, 
and he has found twice as many "paramolar tubercles" in the second 
molar as in the third. The supernumerary posterior of the third 
molar he terms the "distomolar," and finds that when fused, it 

1 For the many beautiful illustrations enforcing this conception the reader is 
referred to the article in Dental Cosmos, February, 1914. 



196 MALFORMATIONS AND ANOMALIES OF THE TEETH 

Fig. 206 




Paramolar fused to third molar. 
Fig. 207 




Paramolar fused. 
Fig. 208 




Paramolar fused to bicuspid. 
Fig. 209 




Fused distomolar in the mandible. 



MACROSCOPIC MALFORMATIONS 197 

unites with the distolingual section of the third molar. He has noted 
a rare case having both a paramolar and distomolar. He also has 
not observed independent paramolars in the mandible, but the para- 
molar tubercle may occur on the second or third molars, which may 
have a proper " paramolar root." The distomolar in the mandible 
fuses with the distolingual portion of the third lower molar. He 
calls attention to the fact that in the maxilla, the paramolar appears 
most often as a supernumerary tubercle, while in the mandible it is 
emphasized by a supernumerary root. 

Fig. 210 




Two atypical upper supernumerary teeth displacing the incisors. 

Bolk regards the appearance of these supernumerary molars as 
thus subject to a certain degree of genetic regularity. The fact 
that one of the writer's patients had a free paramolar in the same 
location on both sides, both alike in form, shows some tendency to 
type. No family history was obtainable. A sister two years 
younger has none. 

In several cases, however, of fused para- and distomolars the 
condition has been unilateral. 

Supernumerary Teeth. — Any teeth in excess of the normal number 
of teeth belonging to any one class are included in the category of 
supernumerary teeth. The number of teeth may possibly not exceed 
thirty-two. Supernumerary teeth appear as simple unmodified 
cones, or as combinations of cones resembling the forms of teeth. 
The. conical form is most common. Cases where these peg-like teeth 



198 MALF0RMAfI0N8 AND ANOMALIES OF THE TEETH 

appear around the third molars, singly or in number, are numerous. 
Their appearance in any situation is evidence that the normal number 
of dental cords has been exceeded. 

Guilford 1 divides supernumerary teeth into those having typical 
anatomical forms and those having atypical forms. 

Supernumerary incisors having typical forms appear in either 
jaw. In the upper jaw, supernumerary centrals and laterals both 
appear, the latter more frequently (Fig. 171). Supernumerary teeth 
may occupy any position relative to the dental arch, but are more 
frequently seen at its lingual side. The compound cone occasionally 
appears (Fig. 211). In addition to molars and incisors, supernu- 
merary bicuspids are occasionally found (Fig. 79) ; supernumerary 
cuspids are very rare, but sometimes a brood of them exists, as many 
as seventeen fairly defined small teeth having been removed from a 
cyst in the location of the cuspid tooth. 2 

Fig. 211 



The compound cone. 

Unless supernumerary teeth are a source of offence, either through 
their position or appearance, they need not be disturbed. If they 
are found to be so, they should be extracted. In the case of a patient 
having had five supernumerary teeth descend one at a time several 
years apart, the last (at about forty years) descended labially, 
appearing at the middle third of the right central root against 
which it pressed, forcing the central lingually so as to also force the 
lower central and lateral inward. The force of erupting teeth is 
thus shown. 

1 American System of Dentistry, vol. iii. 

2 Bundy Allen, M.D.: Jour. Am. Med. Assn. See Dental Cosmos, 1918, p. 636. 



SECTION IV. 

ACQUIRED NON-SEPTIC AFFECTIONS OF THE 
ENAMEL AND DENTIN. 



CHAPTER VL 
ABRASION, EROSION, AND MECHANICAL INJURY. 

Fokmed by the ameloblasts, which are later changed into Nasmyth's 
membrane, and borne upward with the crown during the process 
of eruption (Fig. 186), enamel has no posteruptive source of 
nutritive supply from without. 

Its only conjectural source of nutrition is, therefore, from the 
pulp via the dentinal tubuli. This seems to have been proved by 
Caush, and later by others. (See page 145.) Teeth do change in 
color with advancing age, generally becoming yellower; this is prob- 
ably due to tubular calcification (which see), rendered possible by the 
tubes containing organic matter which are now supposed to permit 
a slow interchange of nutritive sap. 1 It has been shown by Gies 
(see page 145) that even enamel can be permeated by fluid. This 
coloration may be seen in cases of abrasion and in some cases extends 
even into the secondary dentin associated. The editor has a patient 
with a vital tooth of mahogany brown color, which she claims changes 
the depth of color. Changes in the color of the dentin may be trans- 
mitted through enamel, which is normally almost or even quite 
transparent. Such a transparency may be seen at the incisal edges 
of|thin incisors before these edges are worn down. Another proof 
of transmission of color through enamel is seen in caries; a bluish- 
black or white appearance is caused by the decayed ma s or decalcified 
inner surface of the enamel. 

Again, amalgam or gold, oxyphosphate or oxychlorid, reflects its 
color through enamel, and, in excavating, the shadow of the excavator 
may be seen through thin walls. Enamel may be stained or whitened 
by decalcification due to causes acting externally. Extreme polishing 

1 C. Francis Boedecker: Dental Cosmos, September, 1911. 

(199) 



200 XOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

may also cause a new character of light reflection, simulating a change 
in color. Talbot claims a change in color of teeth during prolonged 
illness, such as pneumonia, typhoid fever, syphilis, tuberculosis, and 
in pregnancy. 1 With advancing age, the translucency of teeth 
verges more toward transparency — apparently a sclerotic change 
in the dentin. (See Transparency.) 

After implantation, a tooth may somewhat change its color, but 
this evidently cannot be due to nutrition from the pulp, as this 
organ will have been removed before implantation. It would seem 
that it may take up coloring matter from the saliva. In this con- 
nection the brownin of Black should have consideration. Its appear- 
ance in mottled teeth some time after eruption points to the possibility 
of infiltrations from without. (See page 157.) 

Enamel may suffer mechanical and chemical injury, but whether 
it may undergo constructive changes or retrograde metamorphosis 
is at present only conjectural. There is, however, a possibility 
that a molecular change may occur as a result of slow interchange 
of fluid, environment, or impact of mastication. 

The dentin and cementum contain about 28 and 30 per cent, of 
organic matter, respectively, and stain deeply and permanently with 
great readiness. 

Possessed of living cells, they also undergo changes in their structure 
under the influence of various stimuli, their substance being added 
to or reduced according to circumstances. They are also acted upon 
by mechanical and chemical agencies, if exposed to their influence. 

ABRASION. 

Abrasion is the mechanical wearing away of tooth substance. 

Occurrence. — It occurs most commonly upon the occlusal surfaces 
of teeth, but is also found upon the approximal and labial surfaces, 
the labial cervix, and more rarely upon the lingual surfaces. It is 
also seen in the temporary denture, especially in the molars, and 
is found in animals (Figs. 224 and 225). 

Appearance. — Purely abraded surfaces present a smooth, flat, or 
concaved, highly polished appearance. The surface may become 
stained or otherwise altered in color, or subsequent caries may 
remove its smooth surface. 

Occlusal Abrasion. — Occlusal wear is very common, and occurs 
largely with men who chew tobacco; the contained silex, being gritty, 
acts as an abrasive. Such wear, due to the use of hard food or gritty 

1 Dental Cosmos, 1905, p. 29. 



ABRASION 201 

substances, is seen in skulls of aboriginal man. Ottofy describes a 
peculiar form of wasting due to chewing betel nut mixed with bay 
leaves and slaked lime. No doubt a gritty element is introduced. 
An example of wear uncomplicated by any other possible cause is 
the case cited by Cottingham 1 of a man who wore down two sets 
of artificial teeth "to the rubber and pins" by constantly chewing a 
variety of tobacco said to be usually full of sand. 

Some degree of occlusal wear is accepted as normal to all teeth, the 
act of mastication producing marks or facets at the point of articu- 
lation of antagonizing teeth. A tip-to-tip variety of occlusion 
permits free lateral movement of the lower jaw, and a herbivorous 
type of articulation causing abrasion. It is also frequent in those 
cases presenting the first degree of prognathism. In some of these 
cases, the labial surfaces of the upper incisors and cuspids, and the 
linguo-incisal margins of the lower incisors are worn. A single over- 
lapped lower tooth may abrade an upper tooth in this manner. 

The gritting of teeth is also a cause. This gritting, termed "bruxo- 
mania," may occur only at night or for a few minutes each day; 
again it may appear for entire days, weeks, and months, not ceasing 
even during sleep. In such cases the teeth are worn down flat. 
Maria and Pietkiewicz 2 noted 12 cases of central nervous lesions, 
mostly dementia, developing bruxomania; also it has been noted in 
cases of epilepsy and chorea. A similar condition is the nocturnal 
gritting in children due to rectal parasites as ascaris lumbricoides, 
tenia, etc., or to irritable bladder due to hyperacidity of the urine. 

A clay pipestem may wear a hole of its own diameter in the incisal 
edges of anterior teeth; other stems wear less. Upholsterers and 
seamstresses have peculiar abrasions (tack holding, thread biting). 

The undue loss of posterior occlusion and consequent overuse of 
the anterior teeth cause their abrasion after the manner shown in 
Fig. 212. A marked overbite, produced in any manner, may cause 
lingual abrasion of upper anterior teeth. 

Where the abrasion occurs in a fairly regular manner, four degrees 
of abrasion are classified: (1) Abrasion removing the cusps; (2) 
abrasion removing the occlusal third of the crown; (3) abrasion 
removing the middle third of the crown; (4) abrasion extending to 
the gum line or beyond. (Broca.) (See Figs. 213 and 214.) 

When there is a marked overbite occlusion, with a consequent 
lessening of the lateral movement of the mandible, the teeth do 
not acquire flattened contact surfaces, but their cusps increase in 
sharpness and pointedness. This at times becomes exaggerated, and 

1 Dental Digest, September, 1917. 2 Dental Cosmos, 1907, p. 525. 



202 XOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

Fig. 212 




Abrasion of anterior teeth, with loss of posterior occlusion. (W. A. Capon.) 

Fig. 213 




The first and second degrees of abrasion. Specimens from museum of Philadelphia 

Dental College. 

Fig. 214 




The third and fourth degrees of abrasion. Secondary dentin plainly visible. Specimens 
from museum of Philadelphia Dental College. 



ABRASION 203 

produces an interlocking of cusps or rather worn surfaces which 
have very sharp edges. 

In the first degree of abrasion, the dentin is often hollowed out in 
advance of the enamel of the cusps, forming concave places in which 
berry seeds lodge and cause annoyance. These spots are at times 
hypersensitive. The plane surfaces also are often sensitive upon 
merely rubbing the teeth together. The great majority of worn 
surfaces are comparatively insensitive. Tobacco stains often per- 
meate the occlusal dentin. 

Labial Abrasions. — Some forms of abrasion have been attributed 
to too vigorous use of tooth-brushes, particularly when gritty 
powders are employed. There is no doubt that mechanical abra- 
sion about the necks of teeth is produced in this manner, the gum 
line receding beyond the enamel border, exposing the cementum; 

Fig. 215 




Abrasion due to employment for twenty years of a gritty English tooth paste. 
At 7, gold crown abraded. (Miller.) 



and a careful examination will reveal the cementum and next the 
underlying dentin to be affected; the enamel, when abraded, shows 
first as a facet, then as a spot of bare dentin with thin edges of enamel 
around it (see the left lateral in Fig. 235), and later the area may be 
grooved. As a rule, however, the effect shown in Fig. 234, lower 
jaw, is the more common. These tooth-brush abrasions are quite 
characteristic. In well-kept dentures, the gums are seen to have 
receded from their normal line, but may exhibit little evidences of 
turgescence; the roots of the teeth, upper and lower, are exposed to 
a greater or less extent along their labial and buccal, but not usually 
along their lingual aspects; and they are excavated to variable 
depths, upon the bicuspids and first molars more than upon the 
other teeth, as here the greatest force of brushing is received. The 
upper cuspid is often the first tooth abraded. The depressions have 



204 A OX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

a normal dentin color; sometimes deepened in the mouths of non- 
smokers, especially when brownish secondary dentin is deposited, 



Fig. 216 



A B 




Abrasion of lingual surface by assiduous brushing with tooth powder. At D aDd E 
amalgam worn down. (Miller.) 

the pulp cavity outline often being evident, and which in smokers 
may be periodically blackened by deposits of carbon. If caries 
supervene, the abraded areas lose their normal color, and may be 
readily indented by sharp instruments, which they resist before the 



Fig. 217 



Fig. 218 





Labial abrasion. 



Labial and lingual abrasion. 



advent of caries. The bicuspids and molars, particularly, may be 
grooved in such manner as to require restoration by fillings. 



ABRASION 



205 



Miller 1 investigated this subject very carefully, and found that 
the grit in many forms of tooth powder, vigorously used, was quite 
competent to wear away tooth structure, gold, and other fillings 
(Fig. 219). Figs. 216 and 218 show a lingual wasting, resembling 
graphic erosion. In both cases abrasion is proved by the wasting 
of metal, which acids could hardly accomplish. Crowns and fillings 
may be worn out occlusally, especially if porcelain occludes with 
the crowns and occasionally worn through bucally by brushing. 
Miller experimentally proved abrasion competent to produce the 
grooves known as "wedge-shaped defect" (Fig. 220). 

Fig. 219 




Photomicrograph of sediment obtained by washing tooth paste, which caused the 
abrasion shown in Fig. 215. (Miller.) 



Calculus may be worn in like manner, either by the brush or by 
the festoon of a plate (Fig. 223). 

I have had a case of notched lingual and approximal surface 
on lower incisor cervices due to abrasion by floss silk and tooth 
powder and due to encircling the tooth with floss, crossing the 
ends and pulling each alternately. This was done by my direc- 
tion and the result appeared within six months. While the effect 

1 Dental Cosmos, 1907. 



206 NON-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

was on the cementum and dentin the cervix at the gum line was 
not cleansed as expected. The case taken without consideration of 
cause could have been mistaken for an erosion. 

Fig. 220 




Artificial abrasion produced by brushing with a much-used English tooth paste with 
motor brush for eighteen hours. Remains of gold filling in first bicuspid. (Miller.) 

Fig. 221 




Gradual wear of both tooth substance and filling material, notwithstanding the open 

bite. (Miller.) 



Miller found that among clinic patients who never used a tooth- 
brush the labial abrasion was wanting, and he observed that a 



ABRASION 207 

cessation of wear followed the abandonment of the use of gritty 
powder and the adoption of a soft brush and mild powder, which is 
the evident indication in such a case. 

A clasp may abrade a tooth, and, if food debris be retained on its 
inner side, caries may follow in the abraded area. The purely abraded 
surface will be polished. 

Approximal Abrasion. — Slight approximal abrasion may be normal 
as a facet, due to the rubbing of one tooth upon another at the 
contact point. A marked example of this was seen in the mandible 
of a skull of a Maori. (Museum of Philadelphia Dental College.) 

The third lower molars are locked beneath the distal surface of 
the crowns of the second molars. Some form of bone loss occurred, 
producing looseness of the third molars. The individual motion of 
the teeth produced a deep abrasion of the enamel of the second 
molars upon the distal surface, and an occlusoproximal abrasion of 
the third molars. (Also see Fig. 278.) 

Extensive approximal abrasion may be due to extrusive elonga- 
tion of a tooth in one or both jaws, causing a tooth to occlude with 
its antagonist with a glancing motion. 

In this manner, specimens are produced abraded from the occluso- 
approximal angle to nearly the apex of the root. 

Approximal abrasion by shortening the mesiodistal diameter 
causes the tooth to often occupy a space slightly too large for it 
This leads to food packing, and septal gingivitis or to n on- septic 
pericementitis, bone resorption and looseness. The combined 
causes together with the use of tooth picks leads to a form of peri- 
odontoclasia, often classed as pyorrhea. (The ideas are fully devel- 
oped under the heading of Non-septic Pericementitis.) 

Grit in powder may easily be detected by taking a small portion 
between the incisor teeth, or may be found by elutriating the 
powder, i. e., place in water, stir, let settle for a few seconds, pour 
off the supernatant fluid, and examine the sediment as above, or 
microscopically (Fig. 219). 

Miller found from experiments, as to the effects of various acids 
acting for a time and followed by brushing with abrasives, that it 
depends very materially upon the nature of the acid. Those acids 
which rapidly decalcify (soften) the dentin, of which we may take 
hydrochloric and lactic as types, most readily retard the wearing 
away by friction (unless the friction be so great as to wear in spite 
of the decalcification). While those which act slowly on the dentin 
(oxalic, tartaric, etc.), as well as those which have a macerating 
effect on decalcified dentin, may be wanting in this influence. He 
concluded that wear could not be produced by acid alone, but {hat 



208 XOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 
Fig. 222 Fig. 223 




a, abrasion of lingual surfaces; b, of 
amalgam filling produced by a plate. 
(Miller.) 




Abrasion of calculus. (Miller.) 



Fig. 224 



Fig. 225 




Abrasion of lower incisors of a horse Defects resembling wasting in the teeth 
produced by "cribbing." (Miller, after of a sea lion. (Miller, after Murie.) 

Kitt.) 



ABRASION 209 

any acid or acid salt which possesses the power of extracting the 
calcium salts from enamel, or of breaking up the connection between 
the enamel prisms, may accelerate the process of wasting, provided 
the necessary mechanical factor works together with it. Miller 
found food to be a negligible quantity as to wear upon labial surfaces. 

The editor has a patient presenting the general characteristics of 
Fig. 236, who has been a brush enthusiast, and was taught in early 
life to use a toilet soap containing fine pumice (Bazin's poncine soap). 

The festoon of a metal plate may rapidly cause abrasion of the 
lingual cervix of a tooth. The condition is, however, rare; caries 
being more common. In the editor's practice a case was seen, in 
which several teeth were so affected in a few months, by an ill-fitting 
metal plate. The festoon of a vulcanite plate has also produced 
such an abrasion. 

Abrasion sometimes follows caries, when the latter has become 
freely exposed to attrition. The softened surface wears away and 
the part assumes a polished appearance, but is discolored as the 
result of the stain due to the caries. (See Eburnation.) Also 
caries may follow abrasion at some spot which later escapes the 
constant wear. 

It is probable that a hyperacid condition of the saliva in con- 
nection with mechanical forces may be a cause of rapid abrasion. 
(See Erosion.) 

Effects of Abrasion. — These are external and internal, and most 
marked in the occlusal variety. The crown wears down until at times 
the gum is reached. In the process sharp edges of enamel are formed. 
These splinter off, leaving rough edges, or the enamel may fracture 
or split longitudinally, following the axis of the crown. Supported 
by dentin it does not further break away (Fig. 242). 

Sharp enamel edges may irritate the tongue, producing ulcers of a 
sometimes chronic type, which acquire indurated edges and simu- 
late syphilitic sores or epithelioma. The causal relationship between 
sharp edges of the teeth and lingual epithelioma appears to be quite 
clear in some cases. Brown 1 mentions a case of tetanic spasms of 
masticatory muscles due to this source. 

Sores which have given evidence of malignancy and been diag- 
nosed as malignant growths, have been cured by rounding and 
polishing sharp and irritating enamel edges of teeth. 

The continued stimulation of the ends of the dentinal fibrillar, which 
are exposed in abrasion, causes them either to become hypersensitive 
or stimulates them to formative activity. Tubule material is built 

1 Dental Cosmos, 1908, p. 4. 
14 



210 NON-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

upon the inner walls of the tubule, obliterating their lumen. This 
is the so-called tubular consolidation or calcification (eburnation) . 
Accompanying this, secondary dentin is often formed. As a result, 
most commonly the pulp chamber of the crown is filled up with 
secondary dentin as the abrasion proceeds, and the crown may often 
be worn off until the cervix is reached, while the pulp remains vital 
and covered (Fig. 214). In some cases the abrasion closely ap- 
proaches the pulp, which has failed to protect itself, probably because 
of atrophy of odontoblasts, and the phenomena of hyperemia, or 
even exposure, and its results occur. A left upper bicuspid of the 
second skull in Fig. 214 was in this state. 

Grieves 1 states that ' 'abraded teeth are also affected with 
cemental hyperplasia," which may either be due to mild pulpal 
hyperemia extending to the pericementum, or to reflex irritation, or 
to direct production of mild pericemental hyperemia by strong 
occlusion. 

Fig. 226 




Same case as Fig. 212. Bite opened by bridge-work, posteriorly. Anterior teeth 
restored by means of Land jacket crowns. (W. A. Capon.) 

Treatment of Abrasion. — In the cases of cupped occlusal dentin, 
hard fillings of platinum gold or platinized gold inlays are best. 
Whether the filling be built in or an inlay be set, it is advisable not 
to cut too closely to the enamel in making the cavity, for the struc- 
ture of such a wall is often fractured after filling when this is done. 
If possible the form in Fig. 227, with retention made elsewhere than 
near the side enamel is preferable. Inlays requiring only pin 
anchorage are preferable when undercutting would weaken. 

If nearly all teeth are present and the abrasion slight, bridge-work 
may be used to restore the full occlusion without attempt at restora- 
tion of the worn surfaces. When all teeth are present any causes 
should be stopped if possible and in some cases nothing further 
attempted. 

> Dental Cosmos, 1915, p. 1125. 



ABRASION 



211 



Fig. 227 



If the abrasion of the upper anterior teeth be deep, the bite may 
be raised by appropriate posterior crowns or bridges, and solid 
platinum-gold fillings may be built upon the anterior teeth, either 
the uppers alone or upon both the upper and lower teeth. Anchor- 
age may be obtained in the dentin, or screws may be planted in the 
dentin between the enamel and pulp and the fillings be built about 
them. Instead of malleted fillings, tips of the gold-inlay type may 
be made (Figs. 228 and 229). Casting the 
inlay is a simpler method. Usually it is 
better to use an alloy of iridioplatinum 
gold. This applies also to the lingual 
occlusal abrasion of incisors. 

For those cases in the second degree, 
as a means of limiting the abrasion, Dr. 
J. C. Curry has introduced small trun- 
cated cones of unannealed iridioplatinum, 
which are to be cemented into holes 
drilled into the occlusal faces of the molars 

and bicuspids with an inlay drill of exactly corresponding size, 
mounted in the right-angle hand piece. As many are put in as 
the safety of the pulp and the enamel will permit. They act upon 
the same principle as steel nails in a shoe heel. 




Manner of preparing the 
outer retaining wall of a 
cavity in case of cupped oc- 
clusal abrasion. 



Fig. 228 



Fig. 229 



Fig. 230 






Gold tip for abraded 
teeth with living pulps. 
(Evans.) If cast the mar- 
gins are to be beveled out- 
wardly. 



Gold tip for abraded 
teeth with pulps re- 
moved. (Evans.) 



Porcelain-faced crowns 
for teeth with living pulps. 
(Evans.) 



In other cases, after securing a proper opening of the bite and 
posterior occlusion with crowns or bridges, single porcelain-faced 
gold or platinum crowns may be made to cover each of the anterior 
teeth. For this purpose the crown is appropriately reduced to 
convenient form, but the pulps need not be destroyed. Fig. 230 



212 NON-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

represents the method outlined by Evans. 1 There can be no objec- 
tion to pulp removal in any of these cases, if for any reason a dowelled 
crown seem necessary provided careful canal filling is done. (See 
this and Granuloma.) 

Land jacket crowns, consisting of a wedge-shaped platinum jacket, 
with a porcelain facing attached by means of one of the numerous 
inlay bodies, may be used instead of the Evans crown. In some cases 
other forms of crowns may be indicated (Fig. 226) . 

In raising the bite or for cases in which vital teeth cannot be 
much ground, Dr. Ellwood Garrett has suggested, as valuable after 
long experience, the use of a crown with a cusp made of a single 
thickness 24-gauge clasp metal stamped between a die and counter- 
die of zinc. Xo solder filling is used. 

In labial abrasions approaching the degree shown in Fig. 236, 
screws may be set upon either side of the pulp and silicate cement 
built to the original labial form. Of course if undercuts are per- 
missible and sufficient they may be used. 

There present at times cases of abrasion in which, aside from the 
wear, pyorrhetic conditions may be present, or where bridges cannot 
be properly inserted, especially when only a few teeth remain. 

If this pertain to the upper jaw only, the lower denture may be 
restored to usefulness, the upper teeth extracted, and a full upper 
denture inserted; this permits the adjustment of the bite to any 
desired level. If the conservation of a few teeth is desirable, they 
may be crowned or bridged; the occlusion being raised if desirable, 
then a plate constructed. If the condition be transferred to the 
lower jaw and the anterior teeth be in good condition, a piece with 
the Roach 2 or Morgan type attachment may be fixed upon cuspid 
or bicuspid crowns, but not be allowed to rock with the attach- 
ment as a fulcrum. 

It is to be remembered that in any case of opening of the bite, the 
occlusion is to be restored throughout. 

The bite must not be raised by means of partial plates which strike 
before the natural or crowned teeth, as they tend to embed them- 
selves in the soft tissues and create inflammation. 

If the bite be only slightly raised by plates, this embedding will 
cause a return to the original condition. Sometimes in partial 
cases the natural teeth hold the occlusion while plates unavoidably 
sink. A slight allowance may properly be made for this. Neither 
must too great a strain be placed upon supporting teeth (see Over- 
work of Teeth). In approximal abrasion the indication is its com- 

1 Crown and Bridge Work. 2 Dental Cosmos, 1908, p. 17. 



ABRASION 



213 



pensation by tightening the contacts by fillings, crowns, etc., or in 
some cases united crowns (splints) are necessary. (See Gingivitis.) 

In case of hypersensitivity, Robinson's remedy, silver nitrate, 
nitric acid, or the actual (hot burnisher) or the electrocautery may 
be effective; if not, the areas should be excavated and filled, or, if 
necessary, the pulp should be devitalized. 

If the abrasion be caused by tobacco or gritty powders, etc., its 
use should be stopped. 

A difficult class of cases to treat is found in those highly nervous 
individuals who grit their teeth during sleep. It is probable and 
reasonable that this cause alone may serve to explain abrasions trace- 
able to no other source. The cure of such cases as these could only 
be possible through the wearing at night of some modified form of 
interdental splint. Arnone has described a simple vulcanite splint 



Fig. 231 



Fig. 232 





The "insulator." (Arnone.) 



The " paraglossus. " The metal 
groove shown relates to another 
method of construction. 



for the lower teeth, to open the molars about one-sixteenth of an 
inch and the incisors one-half inch. This he calls "the insulator," 
and is to be vulcanized at 160° C. It is to have the upper surface 
rounded (Fig. 231). He also describes "the paraglossus/' a double 
vulcanite splint made in one piece to be inserted by bruxomaniacs 
during sleep, or by epileptics during the forewarning "aura," if 
present, to prevent grinding or tongue biting. 1 The cases naturally 
indicate the medicinal use of a bromide before retiring, unless the 
causes can be discovered and removed. 

If such gritting be present in children, the evidences of irritable 
bladder, due to hyperacidity of the urine, or of rectal parasites, should 
be sought and treated. The urine may be rendered alkaline by the 
use of potassium salts, and kept so by restriction to a largely vegetable 



Dental Cosmos, 1908, p. 924. 




214 XOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTlrf 

diet. Belladonna may be used to reduce vesical irritability. Rectal 
parasites may be removed by the use of vermifuges, or, occasionally, 
by rectal injections. (See Medical Works.) 

RESORPTION OF ENAMEL 

Definition. — Resorption of enamel is the removal of enamel sub- 
stance by soft tissue containing osteoclasts. 

Occurrence. — It occurs externally only 
FlG - 233 in impacted teeth surrounded, at least 

in part, by irritated tissue, and internally 
very rarely after resorption of dentin by 
the pulp 1 (Fig. 233). (See Pulpitis.) 

Such tissue may also be found in der- 
moid cysts, and causes the resorption of 
impacted cuspid with teeth. (See Fig. 201.) 
resorption of enamel and Pathology and Morbid Anatomy.— Osteo- 

a hematogenic calculus. . 

(Miller.) clasts approximate the enamel as they do 

cementum, decalcify and resorb it. The 
dentin is next attacked. There result irregular excavations (How- 
ship's lacunar) and white or discolored areas of evident slight decal- 
cification of the enamel. A deposition of bone into the area may 
occur. 2 The process is probably the result of a non-septic inflam- 
mation, as in the case of root resorption. (See Interstitial Gingivitis 
and Resorption.) 

The enamel may be resorbed from its internal surface after the 
resorption of dentin by the pulp (see Pulpitis), and, as shown by 
Woods, may be filled in with adventitious material of a structure 
resembling cementum. 

Treatment. — Should the disease by chance occur upon a tooth 
which later has come or been drawn into place, the area may be 
filled; otherwise it has only a pathological interest. 

EROSION. 

Definition. — Erosion of the teeth is a term applied to the chemical 
or chemicomechanical destruction of the hard tissues of the teeth 
in such a manner that broad, shallow, smooth excavations are 
made in the enamel and dentin in situations free from attrition 
by mastication. 3 

1 Hopewell-Smith: Histology and Pathohistology of the Teeth. 2 Ibid. 

3 This term has been much abused and applied indiscriminately to hypoplasias, 
caries, abrasions and the erosions. It seems advisable to restrict it to the above 
dental definition. 



EROSION 



215 



Figs. 234, 235 and 236 illustrate the characteristic appearance of 
such areas. 

The demonstrations of Miller with reference to abrasion of labial 
and lingual surfaces of teeth by means of the tooth-brush and gritty 
powders, and the abrasion of approximal surfaces into grooves in 
animals by the drawing of gritty grasses, etc., through or along the 



Fig. 234 



Fig. 235 




Case described as erosion. (Darby.) 



Case described as erosion (Darby.) 



teeth, or the gnawing of bones by carnivora, etc., have cast a heavy 
cloud of doubt upon the chemical etiology of what have been usually 
considered as erosions due to the action of acid sodium phosphate 
excreted by the mucous glands of the lips or cheek. 



Fig. 236 




4 



A case of erosion (drawn from the cast) : B, silhouette from a perpendicular line through 
the left centrals, upper and lower, showing the loss of substance. (Black.) 



The appearance illustrated in Fig. 234, lower jaw, and in Figs. 
235 and 236 might readily, in the light of Miller's demonstrations, 
be regarded as abrasion, if the causes (brush and abrasive powders) 
he suggests be found; but the graphic outlines shown in Fig. 234, 
upper anterior teeth, seem difficult to harmonize with the abrasion 
theory. The cases of this sort are rare as compared with the others, 



216 X OX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

the editor recalling but two having the peculiar undercut mesial and 
distal erosion borders. The spreading of brush bristles, as the brush 
is brought from the gum down, might account in part for this, but 
in one of the cases mentioned there was also an undercut at the 
incisal border, which would render the theory difficult of application. 

One case was in a man aged forty-five years, a German Jew, 
fond of wines, beer, etc., at meals; the other a middle-aged maiden 
lady of nervous temperament, with whitening hair, slightly wrinkled 
skin, and some evidences of goutiness. 

Black 1 mentions approximal erosions of peculiar type. This is 
very rare at least with me. As stated on page 205 I had a case of 
abrasion due to flossing with use of chalk which looked like Black's 
approximal erosion. 

According to Miller, acids or acid salts, which can extract calcium 
salts, may accelerate the wasting process provided the necessary 
mechanical factor works with it and wears off the decalcified tissue 
before it becomes leathery, when wear is retarded. Kirk burnt 
asbestos cloth, treated it with hydrochloric acid, neutralized this 
with ammonia, washed it with distilled water, and again subjected it 
to high muffle heat. This absorbent, inorganic cloth he applied to 
buccal glands for twenty or thirty minutes in cases of erosion, dis- 
solved the mucus obtained in distilled water, dialyzed the salts out, 
and examined the evaporated residue under the microscope and by 
reagents. He found acid sodium phosphate to be the decalcifying 
agent in what he called graphic (hydroglyphic) erosions (Figs. 234 
and 235). 

Head 2 found by experiment with a 1 to 20,000 solution of acid 
sodium phosphate in water, acting in the incubator at body temper- 
ature, that superficial decalcification of enamel occurred after four- 
teen hours, and when polished off it again decalcified in eight hours, 
and was quite superficially decalcified in two days; that a 5 per cent., 
2 per cent., 1 per cent., and 1 to 500 solution acted under similar 
conditions in seventeen hours, and points out that a solution of 1 
to 10,000 and 1 to 20,000 acid sodium phosphate in alkaline saliva 
acted after eight and five days only. He also has shown that enamel 
which was experimentally slightly decalcified, again hardened when 
placed in saliva for a time. He was, however, unable to explain the 
result. 3 

Miller found the slowly acting acids do not produce such decalci- 
fication as to retard the abrasive action of brushing with a 10 per 

1 Operative Dentistry, vol. i. 2 Dental Cosmos, 1907. 

3 Ibid., 1910, and other interesting facts pointing to the same conclusions in his 
text-book Modem Dentistry. 



EROSION 217 

cent, pumice. Given, then, a decided production of acid sodium 
phosphate by the buccal glands in contact with the labial surfaces 
of teeth (Kirk) for eight hours (the period of sleeping, and Head's 
period of one experiment, see above), it is quite reasonable to suppose 
that an undetermined percentage of acid sodium phosphate dissolved 
in buccal mucus, which in total has an acid reaction to litmus (Tru- 
man, Kirk, and others), is competent to produce a superficial decal- 
cification, which the morning brushing will remove. This repeated 
for months or years may produce the effect seen. Brubaker, in 1894, 
immersed a tooth for a week in a solution of acid sodium phosphate, 
subjecting it daily to tooth-brush friction, and at the end of that 
time spots and grooves resembling erosion made their appearance. 

According to Head and Kirk, the acid phosphate does not attack 
the enamel so as to roughen it, but leaves it translucently smooth and 
white, and this mildness of the action of the acid sodium phosphate 
is just the action that would make smooth erosion with a minimum 
of abrasion. (See Miller's experiments, p. 207.) 

Head points out "that 1 to 500 lactic acid in water will decalcify 
enamel in thirty minutes, while the same percentage in saliva does 
not do so in fifteen days, but that the inhibitory effect of saliva is 
overcome when the lactic acid has a strength of 1 per cent." The 
inhibitory effect, therefore, seems to lie in the relative relations of 
the acid and alkaline element, though Head has shown that a mix- 
ture of 1 per cent, solution of acid sodium phosphate with a 1 per 
cent, solution of tribasic sodium phosphate, which is capable of 
turning blue litmus red, but not of turning red litmus blue, placed 
the acid under control so that the mixed solution did not corrode 
the tooth placed in it, which a 1 per cent, solution of acid sodium 
phosphate in water would do. 

Regarding the production of the abnormal exudate from the labial 
glands, Kirk argues that in diseases of suboxidation (resulting in 
hyperacid conditions such as gout and rheumatism) the blood is 
loaded with carbonic acid as a result of faulty metabolism. In the 
epithelium of the kidneys, the mass action of the carbonic acid upon 
the sodium phosphate of the blood, normally produces acid sodium 
phosphate, which is eliminated in the urine, and sodium bicar- 
bonate, which is returned to the blood and maintains its alkalinity 
according to the following reaction: HNa 2 P04+H2C03 = H 2 NaP04 
+HNaC0 3 . If the amount of carbonic acid be of only normal pro- 
duction, this action will result in only a normal amount of acid 
sodium phosphate in the urine and perspiration; but if in excess and 
not cared for by the lungs, skin, and kidneys, the buccal glands 
may also take up the action and excrete acid sodium phosphate 



IMS XOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

in an identically similar manner. The acid calcium phosphate is 
also found in the saliva at times, and can be formed in a similar way, 
the calcium phosphate being substituted for sodium phosphate as 
the basic salt. 

Kirk states that in the saliva of arthritics there are frequently 
found acid salts, such as acid sodium phosphate and acid calcium 
phosphate. The excessive amount of carbonic acid accounts for the 
excessive loss of phosphate in the kidneys seen in arthritics, as the 
acid sodium phosphate and acid calcium phosphate require for their 
production the basic phosphates, and the elimination of those, con- 
tinuously, produces a phosphaturia until depletion of phosphates 
occur, when their amount lessens and other salts appear. 

In a paper published in 1902, Kirk 1 describes polariscopic obser- 
vations made upon saliva from a patient afflicted with a general 
erosive wasting of the teeth. The patient had had attacks of in- 
flammatory rheumatism, and suffered from obstinate constipation, 
periodic attacks of migraine, headaches, and neuralgia, and his 
saliva was most acid at night. The saliva was dialyzed, the dialysate 
concentrated, and found to contain lactic acid salts, calcium lacto- 
phosphate, calcium lactate, and magnesium lactophosphate (Fig. 237). 

In view of these two classes of cases, Kirk has suggested that 
erosion cases may be of two kinds: (1) A general erosion, in which 
all of the surfaces are uniformly involved, and in which lactic acid is 
the solvent agent; and (2) cases distinctly due to an exudate from 
abnormal buccal glands or gland, the acidity of which is due to either 
acid sodium phosphate or acid calcium phosphate. Talbot 2 claims 
that the systemic acidosis produced by various diseases and by fruit 
eating in excess is responsible for the acidity of the buccal mucus 
and saliva, and for pulp and gingival degeneration and resorption 
through a process of artery and nerve-end degeneration. A decrease 
in the normal acidity of the urine (below 30) indicates renal insuffi- 
ciency, and the difference indicates the amount retained in the 
system. An excessive acidity of the urine indicates excessively 
imperfect oxidation. This expression of the cause is quite compatible 
with the view of Kirk, and both are views of general malnutrition. 

The disease appears to affect females more than males; appears 
usually after thirty years of age, and often some history of goutiness, 
arthritis, or rheumatism can be obtained. Miller denied the presence 
of this disease in the gouty, but since his observation the writer 
has had several patients hold up gouty fingers when questioned as 
to a possible gout as a cause of the erosions present. 

1 Items of Interest. 2 Dental Cosmos. December, 1907. 



ftROSIOtt 



219 



There are other theories which do not seem to be tenable. In 
many cases that have progressed to a marked degree the process 
seems to have ceased spontaneously. 



Fig. 237 




Crystallization of salts from dialysate of saliva from erosion case, showing two typical 
forms. Large crystal is calcium lactate. (Kirk.) 



Fig. 238 




Another field from the same specimen as Fig. 237, also showing two typal forms. 
Large crystal is calcium lactate. (Kirk.) 



220 XOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

Erosion Due to Extraneous Acids. — Miller 1 describes a case re- 
ported by Davenport, 2 of Paris, of a healthy man whose teeth were 
eroded and worn away by acid vapors, within six months of entering 
a factory devoted to the manufacture of nitric and sulphuric acids. 
This effect was observed upon the other workmen also, and also in 
workmen in a dynamite factory in which these acids are used. The 
teeth were first set on edge. Miller suspended a tooth in a flask con- 
taining equal parts of nitric and sulphuric acid, and found that the 
vapors attacked not only the inorganic but the organic portion as 
well, so that upon slight rubbing with a soft tooth-brush the tissue 
was worn away, leaving a hard, polished surface. Miller states that 

Fig. 239 




Crystallization from solution of a tooth in 1 per cent, lactic acid, 
calcium lactate. (Kirk.) 



Large crystal is 



the vapor is nitrogen peroxid, N2O4. Lemon juice, even in lemonade, 
and vinegar will produce this effect of setting on edge, which undoubt- 
edly is due to the chemical solution of a small portion of the enamel, 
probably the interprismatic cement substance, leaving the enamel 
globules a trifle higher, this soon being worn off to a general level 
again. 

Guilford 3 mentions a case of erosion caused by shaddock (grape 
fruit) eating. Tomes cites cases of erosion caused by lemon and 
grape sucking. The pitting of grapes has produced cases of peculiar 



1 Dental Cosmos 1907. 
3 Lectures. 



2 Transactions American Dental Association, 1881. 



EROSION 221 

erosion of the labial and lingual surfaces and incisal edges of anterior 
teeth. In one case in my practice, the incisal anchorage of an 
approximal gold filling was almost worn away upon the tooth most 
used to pit the grape. Unquestionably, other fruit juices or acids 
might act in a similar manner if the acid has an affinity for tooth 
structure, and the exposure to its action is sufficiently lengthy and 
often enough repeated to produce effects. 

The Effects of Erosion. — Tubular calcification and secondary dentin 
are produced together with atrophic changes in the pulp, due to 
secondary dentin formation. Gold and amalgam fillings are left as 
raised islands by the wasting of the tooth around them, though 
Miller has shown that associated abrasions may cause their wear, 
which acids evidently can hardly be expected to do. 

Scratches shown as lines and Baume's clefts are explainable upon 
the theory of abrasion by brush and powders; though usually trans- 
verse, there are sometimes vertical lines. The stimulation of the 
dentinal fibrillar by acid or mechanical stimuli may cause great hyper- 
sensitivity; as a rule, however, this is not pronounced (Fig. 240). 

The anterior teeth are sometimes shortened so that their occlusion 
is lost. Kirk's lactic acid case was of this order. The carious process 
may become implanted upon an eroded area, or at some part of it, 
usually the cervical portion. Whether this is initiated by a decal- 
cifying process due to the acid sodium phosphate, or uncleanliness 
due to a cessation in the intensity of the brushing or due to imperfect 
brushing at this point as is common in most teeth, is not so clear as 
it formerly seemed, when it was thought due to a temporary cessation 
in production of acid sodium phosphate, which was regarded as 
immunizing the part to caries. In any event the stain of iodin is 
taken, showing the presence of bacterial films at the point showing 
caries. 

Diagnosis. — The presence of the peculiar excavations, the hyper- 
sensitivity of dentin if any, and the acid character of the mucus 
from the follicles, as shown upon test with litmus paper made just 
after rising, 1 are diagnostic signs in cases of acid buccal mucus. 
Kirk's* method of obtaining the acid may be used. (See p. 216.) 
The acid reaction is not marked during the day. The writer would 
suggest that on rising the mouth be neutralized with sodium bicar- 
bonate and then washed with water. The patient is then to apply 
the litmus with clean fingers to the glands for ten minutes and 
preserve the litmus for examination. This will give the acidity of 
buccal mucus if present. If found, disease of suboxidition may be 

* Truman. 



222 NOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

suspected and a urinalysis made for confirmation of the general 
symptoms. If not found, habits of fruit use, occupation, etc., may 
be looked for or looked into as a first suspicion. 



Fig. 240 




EC 



Sagittal action of human incisor prepared by Hopewell-Smith's process, and stained 
with hematoxylin: E C, erosion cavity, on surface of which can be seen Baume's 
clefts; P, pulp tissue undergoing degenerative changes; F C, atrophic odontoblasts; 
S D, secondary dentin. X 45. (Hopewell-Smith.) 

Thirdly, general acidity of the saliva on rising or during the day 
may be determined by test repeated by the patient. 



EROSION 223 

Fourthly, sialo-analysis as given by Kirk may be resorted to. 

Failing in these to determine acid as a cause, the case may be 
considered one of pure abrasion, especially if gritty powders, etc., 
are used. 

Treatment. — The treatment of a true erosion if diagnosed as above 
divides itself under two heads: Prophylactic and restorative; the 
prophylactic is again divided into local and general treatment. The 
problem of eradicating the cause of the disorder lies in a correction of 
the morbid glandular secretion. It is evident that if the irritation 
and altered secretion of these glands be due to some systemic cause 
a disease of suboxidation, notably an affection of the gout order, a 
cure of the local disturbance involves the cure of the underlying 
systemic cause. Talbot 1 reduces the acidity to normal with sodium 
bicarbonate (10 to 30 grains), or sodium chlorid (45 grains), after 
meals; or sodium phosphate morning and evening. One-tenth 
grain of calomel is given each two hours, for a time, to cleanse the 
bowel and stimulate the liver. Eight to ten glasses of water should 
be taken daily. A practically antigout diet and hygiene are suggested 
to increase oxidation and elimination. 

Kirk, 2 working to the end of reducing acid buccal secretion, uses, 
three times a day, T ^ grain pure phosphorus in olive oil, in gelatin 
capsules, along with a very mild laxative, and when the urine shows 
a deficiency of phosphates, 25 to 30 grains per diem of glycerophos- 
phate of lime and soda are given. 

Next in importance to the prevention of acid formation is its 
neutralization. This implies the application of alkalies or the use 
of alkaline mouth washes. The greatest production of acid occurring 
during the night, applications of adhesive masses of alkaline sub- 
stances are made to the teeth at night. The principal of these is 
prepared chalk, calcium carbonate; it is rubbed over the labial faces 
of the teeth and between them, before retiring. It remains in 
sufficient amount to neutralize any acid substances coming in contact 
with it. 

Excellent results, as to the checking of the progress of the decal- 
cification, are obtained from the use of magnesium hydrate held in 
suspension in water, or milk of magnesia. Kirk found that three 
hours after the use of a teaspoonful of the milk of magnesia, the 
saliva maintained an alkaline reaction. It should be used at night 
as a wash, after cleansing the teeth, the residue to be left as an 
alkaline coating upon the teeth. The chalk and milk of magnesia 
may be mixed into a paste. If the preparation be disagreeable, a 

1 Dental Cosmos, December, 1907. 2 Dental Cosmos, 1908, p. 811. 



224 XOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

few drops of essential oil may be added. (See Caries.) The induce- 
ment of a flow of alkaline saline by the use of acid fruits at the end 
of a meal may be an aid. The idea is elaborated under the subject 
of dental caries (see Index). The abrasive factor and its possibilities 
as causes of apparent erosions suggest the avoidance of any strongly 
abrasive powders, or, perhaps, a confinement to the use of castile 
soap, Bazin's carbolic acid soap and a soft brush. The hypersen- 
sitivity, if any, is largely controlled by those means though potas- 
sium carbonate in glycerin, tannin in glycerin or Robinson's remedy 
may be used. (See Hypersensitivity of Dentin.) 

It has been suggested by Ottolengui 1 that in the earlier stages an 
impression and plaster model of the teeth be made for comparison 
at future dates, so that the progress of the erosion may be noted. 

Restorative Treatment. — If the eroded areas be excavated and 
filled, the erosion may proceed about the edges of the fillings. It 
may, however, take some time for the erosion to become as deep as 
the original area. 

If metal be used, the margins must be extended to avoid this, if 
possible. Metal is very unsightly in many locations peculiar to 
erosion, so that porcelain inlays, which the locations favor, are 
indicated. The thinness of the porcelain and change of color by 
underlying zinc oxy phosphate indicate the use of a silicate cement 
as the lute in some cases. In their place silicate cement fillings may 
be used, but must be constantly kept in a good condition of surface 
or they become unsightly. 

They last best when placed under the rubber dam. The writer 
has a case of six upper teeth (the cervical half of the teeth involved) 
in splendid condition after five years of service. Screws may be 
introduced to hold the silicate in the flatter erosions. (See 
Abrasion.) 

The generally distributed erosions are only amenable to the prophy- 
lactic treatment (except by crowning, when teeth are largely wasted 
away), and slight erosions are best treated in the same manner. If 
a sharp edge be produced it is well to remove it, as lip irritation may 
possibly be a factor in the acid production, and also tends to localize 
the action of the brush bristle. 

MECHANICAL INJURY OF THE TEETH. 

The enamel is a material much more brittle and inelastic than the 
dentin, and, therefore, less capable of resisting a parting strain. 

1 Methods of Filling Teeth, 



MECHANICAL INJURY OF THE TEETH 



225 



Fig. 241 



Under ordinary circumstances, however, well-formed enamel dis- 
tributed over sound dentin resists all the ordinary forces brought 
to bear upon it. 

Under abnormal conditions, however, enamel appears to fracture 
readily. Dentin may apparently fracture in any plane. 

Causes. — The teeth may be mechanically injured by (1) the action 
of abrasion, which mechanically wears away the teeth; (2) by the 
application of undue force during mastication or by the improper 
use of cutting, filling, or extracting imple- 
ments; (3) by blows of some sort, delivered 
either directly upon the teeth or through forc- 
ible closure of the jaws, as the result of a 
shock or blow delivered upon the rim of the 
jaw. Possibly by expansion of gases or root 
fillings causing pressure from within. (See 
Putrefaction of the Pulp.) 

Aside from blows or bites of sufficient 
force to break sound teeth, it is rare to find 
teeth fractured without a previously acquired 
weakness in the tooth itself. The causes of 
weakness are several. 

During the course of abrasion the enamel 
is worn to a sharp edge, which is readily 
fractured. Oblique splintering occurs in the 
line of cement substance between the glob- 
ules. Longitudinal cracks from incisal to 
cervix may occur. The enamel edges become 
ragged and further fracture is imminent. 
Thread biting produces a similar but localized 
condition (Fig. 242). 

Caries, by removing the natural support of 
the enamel, renders this brittle material subject 
to fracture in ordinary use. The removal of 

dentin from both the mesial and distal sides of a crown by caries 
— e. g., a bicuspid — renders the buccal or lingual section liable to 
fracture, as the result of a strain delivered between the cusps and 
tending to wedge them apart. This accident is liable to occur in 
proportion to the lessening of the healthy dentin between the cavities 
or beneath the occlusal fissure. An upper incisor so decayed would 
naturally have its labial section fractured away, particularly its 
incisal half; usually with an oblique fracture running to the labial 
cervix. A bicuspid or molar usually splits off obliquely to labial or 
lingual cervix (Figs. 244 and 245). 
15 




Fracture of two year's 
standing with pulp vital 
and a lateral tissue growth 
resembling granulation tis- 
sue covering the-root face, 
would explain how the 
case, Fig. 243, occurred. 
(Macdonald.) 



226 X OX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

The exposure of the dentin of a devitalized tooth to the saliva 
seems to weaken it. 

While these principles are correct, it is surprising to what extent 
enamel undermined by caries may retain its integrity if properly 
supported by an adhesive oxyphosphate of zinc. 

The packing of cohesive gold against frail enamel walls renders 
them liable to direct fracture, or if packed so as to permit leakage 
the wall is further weakened by lactic acid produced upon its under 
surface. Again, the improperly prepared cavity margin may be 
comminuted, a condition favoring the recurrence of caries, or a few 
rods or a section may be cracked off along the margin of a filling. 



Fig. 242 



Fig. 243 






Abrasion associated with fracture of the 
enamel. 



Root fracture and reattachment by ad- 
ventitious dentin. (From a specimen.) 



Gold does not support enamel walls so well as oxyphosphate. If 
built over comparatively frail walls in such a manner as to protect 
them from direct impact, they stand fairly well. Inlays of gold 
serve a useful purpose in this connection. 

Some amalgams by attendant leakage permit gradual weakening of 
frail enamel walls. The use of a cement lining, as in combination 
fillings, is distinctly useful both as a support and prevention of 
leakage. 

Johnson 1 explains fracture after filling, where the enamel walls 
were previously undermined but not fractured, upon the theory that 
previous to filling, the pain attendant upon mastication brings about 
a temporary disuse of the diseased tooth. After filling, comfort 
ensues, the patient again uses the tooth, and fracture occurs. He 2 
suggests the successful measure of cutting away frail walls and 
letting the strain come upon the filling. This cannot always be 
done. In many cases of approximal cavities as in incisors, cracks may 



1 Principles and Practice of Filling Teeth. 

2 Text-book Operative Dentistry. 



MECHANICAL INJURY OF THE TEETH 



227 



be seen involving the incisal boundary. In such cases the support 
of cement replaced if necessary often tides over a case for many years. 

The fractures caused by blows present features of interest. An 
actual splitting off of one of the angular portions of a crown may 
occur, or a fracture may be seen resembling one sometimes seen in 
a pane of glass, the result of a light blow from a stone. 

In the latter case, the cracks radiate from a central crushed spot, 
and may involve only the enamel. A large section of an incisor may 
be fractured away and include the labio-incisal third and all the 
lingual section of the crown and a small, obliquely fractured portion 
of the root. This results from a blow — the exact opposite usually 
results from occlusal strain. 



Fig. 244 





Oblique fracture. 



Fracture involving the bifurcation of the roots. 



Longitudinal cracks in the enamel of otherwise fairly sound teeth 
occur, the line running from the labial edge of the gum to the incisal 
edge of an incisor (Fig. 242), or from the fissure of a bicuspid along 
the enamel to the summit of a cusp, or from the cervical margin of 
an approximal cavity to the gum margin. 

These lines probably indicate that force has been applied, sufficient 
to cause a parting of the enamel cap without loss of continuity in 
the more elastic dentin. Dryness from mouth breathing may be a 
possible cause of cracks, and the contact of excessively hot or cold 
substances has been advanced as an hypothesis, but mostly they are 
found in cases of overworked teeth. Flagg alternately plunged 
teeth into boiling water and melting ice without producing cracks, 
while dryness caused them in the same teeth. In some cases the 
enamel cracks may be very numerous. The large cracks take up 
stains, the finer ones do not, as a rule, and can often be seen only 
by throwing the tooth into a shadow by means of the finger, and at 
times in the preparation of cavities, cause annoyance by centring 



22$ XOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

the chisel and perpetuating a defect, necessitating the removal of 
much tooth tissue or the risking of future caries. In one case typical 
of a class of accidents, the root of a second bicuspid was found loose 
and fractured longitudinally (Fig. 246). As its occlusal end was 
firmly embedded in an encircling crown band, and no pins had been 
used, the only explanation seems to be, fracture in preparation, the 



Fig. 246 



Fig. 247 





Case of root fracture. (See Text.) 



Fracture of portion of upper cuspid, 
cause unknown. (Radiograph by E. Ball- 
ard Lodge.) 



swelling of the guttapercha root canal filling or the expansion of gas. 
Such an explanation could not apply to the fracture in Fig. 247. 
Occasionally a root of a multirooted tooth is separated from its 
crown by fracture even when not weakened, though usually caries 
has acted. Sudden twisting seems to be the cause. 



Fig. 248 



Fig. 249 




*1h* 




Fractured molar root. 



Longitudinal fracture of molar root. 



A peculiar case is shown in Fig. 250: A radiograph of longitudinal 
fracture not in evidence until the picture was taken. There was no 
soreness and no fracture of the crown though largely filled. It was 
merely suspected of apical granuloma. (See granuloma for further 
remarks.) Fig. 249 shows a peculiar longitudinal fracture. 

The case in Fig. 248 shows a fractured root, the crown being intact. 



MECHANICAL INJURY OF THE TEETH 



229 





Fig. 250 




r 




•^ 


'1 


MB 


1 



Lo: 



itudinal fracture of mesial 
root cf molar. 



Fracture and repair of enamel after eruption is not, so far as I 
am aware, known. Cases of fracture and repair of dentin have 
occurred. 

A case of such repair by adventitious (secondary) dentin has been 
recorded by Tomes, 1 and Fig. 243 illustrates a fracture of the root 
well below the gum line. The root is girdled by the line of fracture, 
but the dentin has been repaired, and 
the attachment is firm. The line evi- 
dently indicates a repair from the pulp 
side. In a case reported by Val. Mac- 
donald, 2 of a similar fracture, the pulp 
maintained its vitality in both crown 
and root for two years, and until the 
tooth was extracted. There was be- 
tween crown and root, a growth of soft 
tissue connected with both ■ the pulp 
and the pericementum, and considered 
by Macdonald to be pulpal in origin 
(Fig. 241). Macdonald's case would 

explain that in Fig. 243. A case analogous to healing of a com- 
minuted fracture of a central has been reported. 3 Fig. 250 illustrates 
a peculiar fracture due to an unknown cause. 

In an experimental implantation of a dried tooth, filed to fit the 
socket of a previously extracted tooth, union of osseous nature took 
place, and a slight fracture of the root was reunited by osseous 
deposition. 4 

Treatment. — The treatment of fractures involves considerations 
purely operative, and depends upon the nature of the case. Rough- 
ened, abraded enamel margins are best rounded with carborundum 
stones or coarse sand-paper disks, and should be polished. Ragged 
teeth are thus much improved in appearance and resistance to 
further fractures. Sometimes a deep serration must be filled; 
corners are to be nearly rounded or restored to contour by fillings 
or inlays, or at times the entire incisal edge is to be ground away 
and the tooth drawn down and retained until firm. 

In case of an uncompleted tooth root, and the pulp not quite 
exposed, a pure gold, all-metal crown is to be adapted with or without 
grinding, according to the future requirements, and the root com- 
pletion awaited. For adaptation to the neck the cervical portion 



1 A System of Dental Surgery. (See Secondary Dentin.) 

2 Dental Cosmos, January, 1908. 

3 Watson: Dental Record, May, 1906. 

4 Mendel Joseph and Dessonville: L'Odontologie. (See Cosmos, 1904, p. 1060.) 



230 XOX-SEPTIC AFFECTIONS OF THE ENAMEL AND DENTIN 

may be slit and burnished in. If necessary, the capping of the pulp 
may be attempted as well, for the same purpose. 

After root formation the pulp may be destroyed if desired. If 
conservation of the pulp be not possible, the pulp may be prepared 
for removal by pressure anesthesia or conductive anesthesia, and the 
root filled. (See Root Fillings.) 

Fractures involving the cementum demand either the removal of 
the loosened piece and the construction of a special crown retaining 
a portion of the natural crown as a base, or the removal of all of the 
natural crown and the mounting of a substitute upon the root. In 
some cases the remaining portion must be built up with amalgam 
or in part with amalgam as a base. If the loosened portion be 
retained it is apt to irritate, and in most cases in time cause 



Fig. 251 



Fig. 252 





Oblique fracture of root, with pin and 
amalgam for restoration, ready for 
crowning. (Evans.) 



Screws placed into a fractured root to 
enable the building up of amalagam 
around a waxed pin attached to a gold 
cap. This root is one of four piers 
of a nine-tooth bridge in place ten years 
to date- 



lateral abscess with possible remote systemic complications. These 
should be considered very carefully and contra-indicate most 
attempts. For this reason fractures involving the bifurcation are 
unsuitable. The cuspid root shown in Fig. 252 had an amalgam filling 
in its mesial side until after the cap and band were constructed. A 
temporary crown caused the wall to fracture out, so the plan was 
devised of drilling holes in the root side, tapping them with the How 
tap and placing iridioplatinum screws on both sides of the pulp canal 
groove. The pin and cap were then waxed slightly, placed in posi- 
tion, amalgam built in and when hard, the wax was melted by heating 
the cap and pin, which were withdrawn. After thorough harden- 
ing, the bridge-work was proceeded with. Fortunately the root 
received its strain from the lingual side, which was largely intact. 



MECHANICAL INJURY OF THE TEETH 231 

This case is in good condition after ten years of service. In a case 
of fracture of a portion of root side not of such magnitude the canal 
may be prepared and the walls of the aperture of fracture beveled 
for a gold inlay which may have a pin through its center and extend- 
ing further up the canal than the inlay proper. This inlay if arranged 
to "cope" the root face may have all necessary strength for the 
mounting of a crown upon it. The requirements vary, and must 
have due consideration. 



CHAPTER VII. 

STAINS OF THE ENAMEL AND DENTIN. 

Certain stains are found upon the surface of the enamel and some- 
times penetrating its substance. The calculus sometimes located 
upon the enamel is not included in this consideration, though the 
calculus itself sometimes becomes stained. So far as they have 
been observed, stains may be divided into those of metallic and 
non-metallic origin. 

METALLIC STAINS. 

Metallic stains are those which are caused by the direct depo- 
sition of minute particles of metal, inhaled by workers in the metals, 
in the organic collections upon the surfaces of the teeth, or taken 
into the mouth in various solutions of drugs. 

Copper. — Miller found that "workers in copper, brass, or bronze 
all presented a green stain upon the upper teeth, showing every shade 
of green and bluish-green up to bluish-purple. The latter color pre- 
dominated in rooms where phosphor-bronze was worked." Attention 
is called to the fact that "trumpeters very often show a discolor- 
ation of the teeth." Similar discolorations are sometimes noted in 
proximity to copper amalgam fillings. The presence of copper was 
demonstrated in scrapings from some of the stained teeth, imparting 
a characteristic green color to a Bunsen flame. McGeehee 1 notes 
a case of a metal worker whose enamel was stained and the dentin 
as well, the tooth being vital. The presence of defects or spaces 
containing organic matter is evidenced (see p. 143). Bands or wires 
containing base metals, generally containing copper, sometimes stain 
enamel. 

Iron. — "Workers in iron presented stains of a brownish color." 
As pointed out, "the green salts of iron under the conditions found 
in the mouth would become oxidized and brownish in color." The 
administration of iron salts, medicinally, is believed to produce 
black discolorations, iron sulphid being formed. "Iron deposits are 
usual in the border-line between carious and normal dentin." It is 
believed that the brownish spots frequently seen in connection with 

1 Dental Cosmos, March, 1912. 

( 232 ) 



METALLIC STAINS 233 

incipient or arrested caries of the enamel are due to the formation 
of iron salts. Iron or steel in dentin stains black with iron sulphid. 

Manganese. — Manganese was found in the dark colored deposits 
upon the teeth of herbivorous animals, but as yet not upon those of 
man. The investigator stated "that alkaline saliva may be necessary 
to the production of these deposits." Manganese stains may occur 
from the use of potassium permanganate, manganic oxid being 
formed. 

Mercury. — In cases of prolonged mercurial administration the 
deposits (black) upon the teeth may give the reaction for mercury. 
" If mercury and potassium iodid are given together, the green iodid 
of mercury might be present upon the teeth." It is probable in these 
cases that another discoloring substance may form. There is in 
mercurialism more or less gingivitis; the gums are swollen and 
spongy, bleeding readily. "More or less putrefactive decomposi- 
tion of the albuminous matter present upon the teeth occurs, and 
hydrogen sulphid is formed. Reacting upon the oxyhemoglobin of 
the blood, sulphomethmoglobin is formed — greenish red in concen- 
trated, green in dilute solutions." Miller ascribes the discoloration 
found in conditions of gingivitis from various causes, with lack of 
hygienic care, to a probable reaction between hydrogen sulphid and 
oxyhemoglobin. 

Lead. — Hirt (quoted by Miller) found in cases of lead poisoning, 
discolorations upon the teeth: dark brown at the necks, light brown 
on the crowns, with sometimes a trace of yellowish green. Miller's 
tests (limited in number) showed no lead reaction from the dental 
deposits in lead poisoning. 

Nickel. — Some of the salts of nickel are green. Metallic nickel 
attacked by fluids of the mouth and mixtures of bread and saliva pro- 
duces greenish salts. The entire root of a tooth containing a nickel 
retaining screw has been stained a uniform apple green. 

Silver. — The dentin of pulpless teeth containing amalgam fillings 
is sometimes stained black, owing to the formation of silver 
sulphid. 

The use of silver nitrate as a wash may cause the albuminate of 
silver to precipitate salts of silver upon the teeth. If a cavity be 
touched with silver nitrate and an amalgam filling be introduced, 
the salts of silver will be instantly formed at any point where the 
silver nitrate and amalgam combine. If this be upon the enamel, the 
latter will receive a somewhat lasting black stain. 

The nitrate of silver applied to dentin causes the dentin to assume 
a light yellowish green tinge, and the albuminate of silver is formed; 
later metallic silver is precipitated, the tissue becoming black. 



234 STAINS OF THE ENAMEL AND DENTIN 

Nitsehke 1 has called attention to the possibility of stained roots 
showing through the gums. The Howe method of staining roots 
for sterilization with deposited silver should be used with care as 
per directions to avoid the possibility as well of crown staining (see 
Index). 

Gold. — Gold chlorid stains may be formed during the bleaching 
of teeth containing gold fillings by the chlorin methods. The dentin 
becomes first pink, then violet or purple, then black. 2 They must 
be removed for this method. 

NON-METALLIC STAINS. 

Green Stain. — The most common of green deposits upon enamel 
occurs upon both the temporary and the permanent teeth, particu- 
larly of young persons. The deposits usually have a crescentic form, 
are mainly upon the labial faces of the anterior teeth, and may be 
but a narrow line or may cover one-half the labial face. It is unusual 
for the deposit to extend far into the interproximal spaces, their 
tendency being to follow the edges of the approximal surfaces. While 
green stain undoubtedly does form upon adult teeth (Figs. 253 and 
254), where clearly the enamel cuticle has long been absent, it is only 

Fig. 254 





Extension of green stain on the approx- Extension of green stain on the lingual 

imal surface of the incisors. (Miller.) surface of the incisors. (Miller.) 

very common upon young teeth where remnants of Nasmyth's mem- 
brane persist about their necks. The color of these deposits varies 
from light green to greenish black. 

If an instrument be passed over the portion of enamel affected, 
more or less roughness of the surface is evident. If the deposits are 
subjected to friction with abrasives, they disappear slowly and the 
enamel beneath may be found roughened. This has led to the belief 
that these deposits cause decalcification of the enamel. It is found 
upon adult teeth that when an area of cervicolabial enamel has 

1 Dental Cosmos, 1918. 

2 Kirk: American Text-book of Operative Dentistry. 



NON-METALLIC STAINS 235 

become roughened through slight decalcification, a green stain is 
likely to form upon the rough surface, if proper hygienic care be not 
exercised. It is also found that if the stain be removed by means of 
abrasives, the roughened enamel may be readily polished — i. e., the 
decalcification is very superficial. 

If cases be observed early enough in childhood, it will be noted that 
green stain is usually preceded by a lack of oral hygiene; collections 
of food debris are not removed from about the necks of the teeth, 
which implies that prior to the formation of green stain the aifected 
enamel surfaces have been subjected to the action of fermenting 
food debris — that is, to acids. These facts have led to an acceptance 
of the view that the roughness or decalcification has preceded the 
green deposits, but the writer does not feel certain about this. "If 
teeth be placed in a 10 per cent, solution of hydrochloric acid, in 
from two to four minutes the enamel cuticle begins to loosen, and in 
from five to ten minutes is isolated. It is found that the entire 
stain comes away with the cuticle." 

In even the mouths of children, the removal of green stain with 
pumice may be difficult, showing that some penetration of enamel 
substance has occurred. 

Nature of the Coloring Matter. — The coloring matter is found to 
be insoluble in water, glycerin, alcohol, ether, chloroform, or oil of 
turpentine. Mineral acids, hydrochloric, nitric, and nitrohydro- 
chloric act but slowly upon the coloring matter; even hydrochloric 
acid requires some hours to completely destroy it. Tincture of 
iodin, commonly believed to act as a solvent of green stain, was 
found to affect it but slightly. Both chlorin and nascent oxygen 
destroy the coloring matter rapidly, the cuticle being bleached in a 
few minutes by a 10 per cent, solution of hydrogen dioxid. Thick, 
dark green deposits were incompletely bleached after eight hours' 
immersion in the 10 per cent. H2O2 solution, pointing to a lack of 
uniformity in the composition of the stain. 

The belief that the green coloring matter is chlorophyl is contra- 
dicted by the fact that it is not soluble in ether. 

Miller 1 regarded the association of the green discoloration with 
sulphomethemoglobin, or some allied substance, as the most probable 
explanation, though he found a micrococcus in a deposit of green 
stain which produced a grayish-green color in glycerin agar. 

Miller did not find any definite connection between a milk diet 
and green stain. 

Goadby 2 has found Bacillus liquefaciens fluorescens motilis present 

1 Dental Cosmos, 1894. 2 Mycology of the Mouth. 



236 STAINS OF THE ENAMEL AND DENTIN 

in several cases of green stain. It deposits in its culture medium 
a fluorescent blue-green pigment. Other mouth bacteria produce a 
greenish pigment — e. g., Bacillus pyocyaneus and Bacillus fluorescens 
non-liquefaciens. 1 The Streptococcus viridans produces a green pig- 
ment in some media. 

In case of roughened enamel, green stain appears at times to have 
been taken into its substance, rendering removal without bleaching 
difficult. 

Black Stain. — A peculiar black stain occurs in the mouths of appar- 
ently healthy individuals, both men and women, and smokers and 
non-smokers, and even with those also who drink neither tea nor 
coffee. . It occupies the general position described for green stain, 
but may cover much of the surface of the teeth. It occurs in some- 
what unclean mouths, though the teeth may have been regularly 
brushed. As a rule, those teeth having the deposit are comparatively 
free from caries. Its etiology is not worked out, but it may be due to 
a formation of metal sulphids in place of sulphomethemoglobin. I 
have asked both a bacteriologist and a histologist to examine some 
of this pigment but without result. It is very readily removed, 
and does not, as a rule, affect the enamel. At times a superficial 
caries is found associated with it, and at some minute spot the 
enamel may be penetrated. Whether this cavity is a result of the 
action of the film is not certain. In a case of a woman a black 
stain was prevalent for years — recently it has entirely disappeared. 
The only available explanation other than some possible unknown 
systemic change, is the use of a well-known tooth paste which con- 
tains a large percentage of potassium chlorate. 

Tobacco Stains. — Smokers have characteristic black deposits upon 
both the teeth and calculus deposited upon them. The stain is most 
marked upon the lingual surfaces of the teeth, and a pipestem held 
well back in the mouth may cause a thick deposit upon some of 
the posterior teeth. 

Tobacco juice itself stains exposed dentin and cementum, and 
enters cracks in the enamel, producing brown discolorations very 
difficult or impossible to remove. McGeehee found tobacco stain 
to have deeply penetrated the enamel tissue. 

Stains Due to Dyes. — McGeehee 2 has shown that colored mouth 
washes containing vegetable or anilin coloring matter may stain 
enamel and other tooth structure. The chewing of betel nut or 
other material containing vegetable coloring matter also produces 
a stain characteristic of the coloring element. Dyed cotton also stains. 

1 Mycology of the Mouth. 2 Dental Cosmos, March 1912. 



TREATMENT OF STAINS 237 

The use of dilute Talbot's iodogylcerol while valuable as an oral 
antiseptic has produced unsightly stains, giving a coppery look even 
to gold inlays. 

Red Stain. — A peculiar red stain occurs upon the necks of some 
teeth, but is not generally distributed. It is probably due to 
chromogenic bacteria, as it is only found on unclean surfaces. 

According to Goadby, 1 Bacillus prodigiosus, Bacillus rouge de Kiel, 
Bacillus mesentericus ruber, Bacillus roseus, Sarcina roseus, Micro- 
coccus roseus, and other micrococci produce a red pigment in at 
least some of their media. 

Sarcina lutea and Sarcina aurantiaca produce yellow and orange- 
colored pigment respectively. 2 The exact relation of chromogenic 
bacteria to stains is not worked out. 

DENTIN STAINS. 

Exposed dentin may be stained as enamel is. In addition it may 
take up certain stains like tobacco. 

Metallic fillings, such as amalgam, containing mercury, silver, 
copper or cadmium metals which combine with sulphuretted hydro- 
gen to form sulphids, may cause staining of dentin. 

Metallic posts containing silver, copper, or nickel, or made of 
steel or iron wire, may produce sulphids in the same manner. The 
dentin may also be stained pink by hemoglobin entering the tubules 
during the progress of venous hyperemia. This finally develops 
iron sulphid. The dentin may also be stained by iron sulphid formed 
during putrefaction of the pulp, by the action of ammonium sulphid 
upon the iron contained in the hemoglobin of the blood undergoing 
decomposition. Silver nitrate solutions and Howe's preparation also 
stains dentin. The dentin has been stained by the dye in colored 
cotton. 

TREATMENT OF STAINS. 

Enamel stains are best removed by mechanical means, after the 
removal of calculus from the teeth. (See Salivary Calculus.) For 
this purpose, brush wheels and rubber cups charged with pumice and 
revolved in the dental engine are used to remove the accessible por- 
tions of the stains in obstinate cases. Next a wood point, made by 
sharpening an orange-wood stick or hickory shoe-peg to a wedge- 
shape, is charged with the pumice and rubbed by hand over all the 
surfaces not reached by the brushes and cups. For the more inacces- 

1 Mycology of the Mouth.. 2 Ibid, 



23S STAINS OF THE ENAMEL AND DENTIN 

sible situations, the point is to be mounted in a Jack or other porte 
polisher. A very fine linen tape, a German silver or steel strip, or 
flat floss silk charged with pumice will remove the stains at the con- 
tact points. A very small finishing bur or dull ordinary No. 1 or 
No. \ bur is useful upon lingual surfaces or in grooves. 

The powdered pumice used is best mixed with glycerin, to prevent 
the flying of the pumice during the rapid revolution of the wheels. 
Saturation of the stains with tincture of iodin followed by a douche 
of water renders them more visible, and also brings to view the 
associated bacterial films upon the teeth. A very weak solution of 
hydrochloric acid or ammonium bifluorid (tartasol) may be momen- 
tarily applied and immediately brushed off with the rubber cup and 
pumice. 

Register recommends the use of 1 per cent, hydrogen dioxid, to 
be forcibly sprayed upon the gums and deposits both before and 
after the use of tincture of iodin. The brush and pumice will then 
rapidly remove the stains and bacterial films upon the accessible 
portions of the teeth. 

Tobacco stains in cementum need not be removed to their full depth. 

Head 1 has suggested the removal of deep enamel stains and the 
deposits in irregular depressions and joints of inlays, inaccessible to 
the stick, by the use of nascent oxygen derived from 25 per cent, 
ethereal pyrozone, or a paste of sodium dioxid and water, made by 
dissolving the latter in distilled water at about 32° F. These are 
applied to the part on cotton, and nascent oxygen liberated with a 
hot burnisher. The face and gums are protected by the securely 
placed rubber dam and by oiling the face. 

The method is also applicable to the bleaching of obstinate stains 
of the dentin, especially near the cutting edges. 

In the joints of inlays, fresh cement is to be rubbed — preferably 
the silicates — in order to prevent a rediscoloration. 

If beneath green stains decalcification be discovered, the decal- 
cified area should be polished as well as possible, but not cut away 
unless carious and the patient urged to careful prophylaxis. 

After the removal of calculus and stains from the teeth, the mouth 
and teeth should be kept in as cleanly and aseptic a state as possible, 
by the employment of correct prophylactic measures. Dental caries 
and pyorrhea alveolaris are thus also largely prevented. (See Pro- 
phylaxis of Dental Caries and Pyorrhea Alveolaris.) 

The stains found in the dentin are also divisible into metallic and 
non-metallic. The former are best removed by transforming the 
insoluble metallic salt into a soluble one. 

1 Items of Interest, 1902, 



TREATMENT OF STAINS 239 

The most frequent and practicable course is to form soluble chlorids 
through the action of nascent chlorin. Copper, nickel, gold, and 
iron stains should be subjected to the chlorin method of bleaching, 
followed by repeated washings with chlorin water, 50 per cent., and 
hot distilled water to remove the chlorid formed. 1 

Silver stains are converted into silver chlorid by the chlorin 
method, or iodid by the use of tincture of iodin, and dissolved out by 
the use of sodium hyposulphite, followed by hot distilled water. 2 

For mercurial stains Kirk recommends the use of aqueous, ammo- 
niacal solution of hydrogen dioxid after the chlorin method, and a 
saturated solution of potassium iodid after the iodin method, in 
either case followed by washing with hot distilled water. 

Manganese stain is removable by the use of 25 per cent, aqueous 
solution of hydrogen dioxid, saturated with oxalic acid crystals and 
followed by washing with hot water. 

The non-metallic dentin stains are removable by the use of chlorin 
evolved from chlorinated lime by the reaction with dilute acetic 
acid, or of nascent oxygen evolved from hydrogen dioxid or sodium 
dioxid. 

In either case the color molecule is destroyed by the indirect or 
direct oxidizing effect. 

The hydrogen dioxid may be used in the form of the 25 per cent, 
ethereal solution (25 per cent, pyrozone) applied for a time, or sealed 
within the tooth for twenty-four hours, or the 25 per cent, aqueous 
solution may be driven into the tubuli by the aid of the cataphoric 
current. 

Sodium dioxid should be employed in saturated solution in distilled 
water (made at about 32° F.). The dentin is first desiccated and 
then saturated with the solution. Weak sulphuric acid (10 per 
cent.) is used to liberate the nascent oxygen. Kirk recommends a 
second application, omitting the use of the acid. 

As with metallic stains, all the by-products should be washed out 
with hot distilled water. 3 

A further description will be given under the caption of Putrefac- 
tion of the Pulp. 

1 Kirk: American Text-book of Operative Dentistry. 2 Ibid. 

3 For a complete description of the bleaching process, see Kirk's article in American 
Text-book of Operative Dentistry. 



SECTION V. 

DENTAL CARIES AND HYPERSENSITIVE 
DENTIN. 



CHAPTER VIII. 

DENTAL CARIES: HISTORY; EXCITING AND PRE- 
DISPOSING CAUSES. 

Definition. — Dental caries may be defined as a disease of a tooth 
characterized chiefly by the production of a localized cavity, con- 
cavity, or area containing decalcified tooth structure and due to a 
combined acid fermentation and liquefaction. 

History. — Examinations of crania show the disease to be certainly 
as old as semicivilization, and when more data are obtainable it 
will, no doubt, be found even older. The skull of a mummy in the 
British Museum, dating 2800 B.C., exhibits well-marked caries and 
other dental diseases. Caries appears in the teeth of the skulls of 
all peoples, no matter what their degree of civilization, provided 
their dietary included cooked, starchy foods. 

Causes.— These may be divided into exciting and predisposing. 

Prior to the investigations of Miller, 1 published in 1882, a vast 
amount of labor was expended in the effort to determine the cause 
of dental caries. The deductions made were partly speculative and 
partly based upon scientific investigations. 

From 1754 to 1835 caries was regarded as an inflammation or 
gangrene of tooth structure; Boudett, Jourdain, Hunter, Fox, Bell, 
Fitch, and Koecker advancing one or the other theory. 2 

In 1835 Robertson, 3 of Birmingham, England, advanced the 
opinion, based upon his observations, that it " is to chemical and not 
to inflammatory action that the destruction of the teeth must be 
attributed." The author pointed out forcibly the errors and fallacies 
of previous writers. He stated that "Particles of food retained in 

1 International Dental Journal, 1884. 

2 For an interesting and exhaustive exposition of their views, see American System 
of Dentistry, Section on Dental Pathology, by Black. 

3 A Practical Treatise on the Human Teeth, second edition, Philadelphia, 1839. 

16 (241) 



242 DENTAL CARIES 

fissures and imperfections of the teeth and in the spaces between the 
teeth undergo a process of decomposition and acquire the property 
of corroding, disuniting, and therefore destroying the earthy and 
animal substances of which the teeth are composed." 

John Tomes, a little later, was the first to record microscopic 
examinations of carious dentin. He described the transparent zone 
lying between the carious and non-carious dentin, and observed and 
pointed out also the dentinal fibrillse. He announced the very 
significant fact in relation to caries, that if blue litmus paper be 
applied to a carious cavity it is at once reddened, which furnishes 
evidence of the presence of an agent capable, if unresisted by the 
vitality of the dentin, of depriving the tissue of its earthy constitu- 
ents, leaving the "gelatin to undergo a gradual decomposition 
favored by the heat and moisture of the mouth." 

Tomes first established the essentially chemical character of some 
features of caries. The character of the acid and its localization were, 
however, not ascertained. 

In 1867 Bridgman promulgated the theory that the crown of the 
tooth and the gum were of different electrical potential, and that 
being bathed in the oral fluids, the conditions of a battery were set up. 

Acid substances were said to be set free at the positive pole (the 
crown), causing decalcification. 

S. B. Palmer, in 1874, claimed that after filling, recurrent caries was 
caused by the conditions of a battery being set up — i. e., the differ- 
ence of electrical potential between the filling and dentin in the 
presence of saliva or of the fluid of the dentin, as an electrolyte 
caused liberation of acids, producing decalcification of the tooth or 
disintegration of the filling — e. g., oxyphosphate. » 

Miller, in 1881 and 1900, 1 experimentally examined these assump- 
tions. He ground the enamel away from the crowns of freshly 
extracted teeth and filled cavities made in them with gold and gutta- 
percha. These he placed in separate flasks containing a physiological 
salt solution (0.75 per cent, sodium chlorid). This, in the presence 
of electric currents, should produce hydrochloric acid by liberation of 
hydrogen and chlorin, and decalcification should occur. After four 
years there was no decalcification. 

Similarly filled teeth were suspended in dilute lactic acid. The 
decalcification was exactly similar to that in the unfilled pieces used 
as a control. Had electrolytic currents been generated between the 
metals and dentin, the latter would have been acted upon more 
vigorously than in the unfilled pieces. 

1 Dental Cosmos, April, 1901. 



EXCITING CAUSES 243 

In 1868 Watt 1 advanced the theory that free sulphuric, nitric, and 
hydrochloric acids were generated in the mouth during putrefactive 
processes and caused the different varieties of caries. 

Magitot 2 pointed out that the essential phenomena of caries, as 
they were then understood, were the same in natural teeth mounted 
upon plates as in the natural organs in situ; proving that caries is 
intrinsically independent of existence of vitality. By immersing 
teeth in solutions of sugar undergoing fermentative changes, he found 
that decalcification occurred. Teeth immersed in solutions of sugar, 
in which fermentation had been prevented by boiling the solution 
and sealing, or by additions of sufficient carbolic acid, remained 
unaffected. 

Leber and Rottenstein, in 1867, first called attention to the 
probable causative association of bacteria with some phases of 
dental caries. By staining carious dentin with iodin, the dilated 
dentinal tubules were shown to be filled with granular bodies, which 
they recognized as bacteria, identifying but one of the many forms 
of oral bacteria — the leptothrix. They deemed an initial exposure of 
dentin a necessary preliminary to the invasion and growth of the 
leptothrix, which in conditions of lessened resistance gained access to 
the tubules and in some undescribed manner caused their dilatation. 

The question of the recognition of the presence of bacteria directly 
resolves itself into the subject of special staining. Prior to the work 
of Koch, presented in 1881, no means of isolating specific bacteria 
by special cultures and staining were known, and it is remarkable 
that in the same year, the essential features of dental caries were 
first made out with some degree of clearness. 

Miles and Underwood (World's Medical Congress, 1881) pointed 
out clearly and at length, the different appearances produced by 
simple decalcification of dentin and those by dental caries. Speak- 
ing of Magitot's experiments, they say: "We assume that two 
factors have always been in operation: (1) The action of acids and 
(2) the action of germs. When caries occurs in mouths it is always 
under circumstances more favorable to the action of germs than to 
the action of acids." They believed that the acids necessary for 
the decalcification were excreted by the germs, which utilized the 
dentinal fibrillar as a food supply. 

It will be seen that the invasion and multiplication of organisms in 
the tubuli were held as the antecedent of the process of decalcifica- 
tion. The deductions of these observers were drawn from data 
not derived from the methods of modern bacteriology — i. e., special 

1 Chemical Essays, 1868. 

2 Treatise on Dental Caries, Experimental and Therapeutical Investigations, 



244 DENTAL CARIES 

stains and special cultures. Moreover, they were made before the 
physiological chemistry of bacteria was even partially understood. 

In 1882 W. D. Miller, of Berlin, announced, as the results of 
experiments conducted by him, that he believed the first stage of 
dental caries to consist of a decalcification of the tissues of the teeth 
by acids which are for the greater part generated in the mouth through 
fermentation of carbohydrate food by bacteria. This was in agree- 
ment with the clinical deduction of Robertson, of England. 

The observations of Miller were supplemented by J. Leon 
Williams, who demonstrated a microbic collection upon the 
surface of superficially decayed enamel, and having sufficient 
attachment to permit grinding in situ. Williams claimed that 
these plaques are the primary agents which manufacture acid from 
carbohydrate material in association with them. 

These, and other observers whose names will be mentioned in 
place, have thrown side-lights upon the formation and nature of the 
plaque and upon the pabulum which they require and out of which 
they form acid as one of their by-products. 

The reader will be assisted in considering the somewhat discon- 
nected facts hereafter given by bearing in mind the generally accepted 
theory of the modus operandi of caries deduced from the facts brought 
out and which is now briefly stated. The primary cause of dental 
caries is a collection of bacteria upon the surface of the tooth. This 
probably begins with a coating of the tooth by saliva in which a 
certain proportion of solid organic matter exists — mucin, globulin, 
leukocytes, epithelial scales, etc. 

This is immediately infected by ever-present bacteria, which form 
colonies in it. This mass of organic basis and bacterial colonies 
when firmly established can be ground in situ and constitutes a 
"microbic plaque." By itself this cannot produce dental caries. 
To this microbic plaque comes the carbohydrate food which is the 
second essential factor in caries. 

Kirk 1 states that, owing to the presence of carbohydrate and 
bacteria, lactic acid is formed which precipitates mucic acid out of 
mucin in which it exists in combination with an alkaline base. He 
describes mucic acid as opalescent, adhesive and insoluble except 
in an alkaline or saline solution. 

He states that when caries is in active progress the saliva is 
ordinarily acid in mucin, rendering it ropy. That it is neutral or 
faintly alkaline in reaction. That if lactic acid be added to it in 
a test-tube, mucic acid will be set free as an opalescent precipitate 

1 Chapters on Caries, Femes, Mouth Hygiene, p. 196. 



EXCITING CAUSES 245 

from the alkaline base with which it was chemically combined as 
mucin. 

There was exception taken to this theory by Miller, who claimed 
that plaque formation was not essential, but that the infected food 
mass could form the acid and act directly. This is simply a question 
of whether bacteria act in the mass or under the mass, and is only 
a question of modus operandi, not of essential fact. Pickerill 1 endorses 
Miller's viewpoint, but so far as the writer is aware neither Miller nor 
Pickerill have offered any satisfactory proof that the plaque which 
von Beust has shown to form in a few hours is not the localizing 
factor. There is, indeed, no reason why an infected food mass should 
not form its own underlying plaque out of there existing mucin and 
bacteria. The theory of self solution of base of attachment of the 
plaque (reason 2 2 ) seems weak in view of the rapidity of bacterial 
reproduction. 

In either case after bacterial fixation the carbohydrate is changed 
by the bacteria to acid, mainly lactic acid. This decalcifies the 
tooth substance, leaving the organic matrix. The organic matrix is 
next destroyed by bacteria having the power of its liquefaction, 
probably due to their enzymes. Both the inorganic and organic 
bases of tooth structure being destroyed, a cavity is left. This 
being a relatively slow process, the intermediate stages are found. 

Miller's observations and experiments established the following 
basal facts in connection with dental caries: 

1. That in all cases of dental caries microorganisms may be seen 
under the microscope in the tubules of the carious dentin, and that 
bacteria exist in great numbers in the mouth. 

2. That the invasion of the tubules is always preceded by decal- 
cification of the dentin — i. e., an area, sometimes relatively large, 
of decalcified dentin may be seen in advance of the organisms. 

3. Analysis of the softened dentin proved that a large part of its 
lime salts were removed — i. e., decalcification had occurred. 

4. Test with litmus paper gave the acid reaction in nearly every 
case, so that the inference that decalcification was due to an acid 
was warrantable. 

5. The food substances taken into the mouth are of all classes. 
Carbohydrates (sugars and starches), hydrocarbons (fats), and 
nitrogenous (albuminous) materials. 

The carbohydrates are fermented with acid reaction by many 
mouth bacteria, commonly producing lactic acid; the albumins 
ferment with an alkaline reaction. 

1 The Prevention of Dental Caries and Oral Sepsis, 2d Ed., p. 24. 2 Ibid. 



240 DENTAL CARIES 

It was inferred from this and other experiments that caries was 
due to the acid fermentation of carbohydrates and not directly to 
the fermentation of albuminous substances. 

6. That oral fermentation is the result of bacterial action, his 
following fundamental experiments show: 

(a) A small tube was filled with a solution of starch and fastened 
to a molar tooth on retiring. The next morning the contents of the 
tube had a strong acid reaction. A tube of the starch solution with 
saliva added was incubated at blood temperature. After four or 
five hours the mixture became acid. 

(b) The mixture of starch and saliva was kept at 100° C. for a half- 
hour, and incubated. It did not become acid — i. e., the exposure to 
this temperature killed the ferment. 

(c) The saliva was boiled for a half hour and then added to the 
starch solution and the mixture incubated. No acid was produced — 
i. e., the ferment existed in the saliva, not in the starch. 

(d) The ptyalin of the saliva was destroyed by heating the mixture 
for twenty minutes at 67° C; the incubated mixture still became 
acid — i. e., ptyalin did not act as the acid-forming ferment, but the fer- 
mentation must have been caused by some other ferment not destroyed 
by exposure to this temperature. (Some sugar probably formed.) 

(e) To the mixture of saliva and starch, carbolic acid was added 
as an antiseptic. No acid was formed, but the ptyalin changed the 
starch to sugar — i. e., the acid-forming bacteria were inhibited, the 
ptyalin not. 

(/) A number of tubes were each supplied with a small quantity of 
the saliva-starch solution and sterilized; a third of them were infected 
from the mouth, a third by carious dentin, and a third were left 
uninfected as controls. The infected tubes became acid; the controls 
did not. 

(g) The first of a series of tubes containing sterilized saliva and 
starch solution was infected with carious dentin; when this became 
acid a fraction of a drop was carried from it to a second tube. After 
that became acid a third was infected from it, and so on indefinitely. 

Conclusion. — Carious dentin contains a ferment or ferments cap- 
able of reproduction — i. e., living organisms are present in it. 

7. The nature of this living ferment was determined by infecting 
a culture medium with carious dentin taken from the deeper layers. 
The bacteria cultivated were distended into pure cultures by carry- 
ing through a series of cultures and examining microscopically during 
the process. The same morphological characteristics were exhibited 
in the last tube, as shown by the germs in the deeper layers of carious 
dentin itself, and were identical with that of Bacterium acidi lactici. 



EXCITING CAUSES 



241 



These germs may be found in the sediment of a culture tube, and 
consist of cocci and micrococci, either single or in chains. These 
cocci possess the power of forming lactic acid from glucose. The 
organism is a facultative anaerobe (Fig. 255). 

8. A sound bicuspid was sawed into sections, and an equal number 
of these sections placed in each of two test-tubes. Upon these was 
poured a 2 per cent, aqueous extract of beef (albuminous). To one 
tube a minute portion (0.2 per cent.) of cane-sugar was added. Both 
tubes were sterilized, and after cooling infected with a pure culture 
of the germ, obtained from the deeper layer of carious dentin. The 
sugar-containing solution became acid in a few hours; in a week the 
dentin was softened; in two weeks thin sections were completely 
decalcified; in three weeks cavities were found in the dentin, exactly 
similar to cavities formed in teeth in the mouth and presenting under 
the microscope other phenomena of caries to be described later. 



Fig. 255 



Fig. 256 




A more prolonged fermentation resulted in the complete disintegra- 
tion of the slabs of dentin, a proof of the fact that one organism may 
completely destroy dentin. 

In the tube containing only the extract of beef, no acid was pro- 
duced, and no decalcification of the dentin occurred. 

From these facts, Miller argued that putrefaction does not initiate 
the process of dental caries, and may not be essential to the destruc- 
tion of either the inorganic or organic dental elements. 

9. That the acid produced was lactic acid, Miller demonstrated 
as follows: 

Starch and saliva were mixed and fermentation induced. This 
was then checked by sterilization with heat. A quantity of material 
being collected in this manner, the whole was concentrated by 



24$ DENTAL CARIES 

evaporation, and tested with a solution of methyl violet, which 
would turn first blue and then green with an inorganic acid. Not 
so reacting, and not distilling off during the concentration, the acid 
present was pronounced a non- volatile organic acid. The concen- 
trate was shaken with a quantity of ether, which dissolved the organic 
acid present. When the solution was clear, it was filtered and the 
ether partially distilled off, when the partially concentrated solution 
was further concentrated over a water bath and then mixed with an 
excess of freshly prepared zinc oxid. The whole was boiled, water 
being added as needed, until the solution became neutral, when it 
was set aside to crystallize. A drop placed upon a slide under the 
microscope showed the forms of crystals of zinc lactate (Fig. 256). 

By testing the molecular weight of the washed and dried crystals 
it was determined clearly that the substance was zinc lactate. 

In practically a similar manner, lactic acid was obtained directly 
from carious dentin. 

While Miller demonstrated the ability of one organism to produce 
all the essential phenomena of caries, including liquefaction of the 
dentin, he did not claim that only one or two organisms are involved 
in the process, but that " any germs possessing the power of producing 
acid fermentation of food may and do take part in the first stage of 
caries, and that all those possessing a peptonizing or digestive action 
upon albuminous substances may take part in the second stage; 
and that those possessing both properties may take part in both 
stages." 1 

He was of the opinion that it is not the presence of this or that 
kind of bacterium, but rather the joint activity of the total flora, 
as expressed in intensity of fermentation in food particles, which 
determines the extent of caries. 

Out of eighteen mouth bacteria examined, Miller found ten that 
produced lactic acid in sugar-containing solutions. 2 He also found 
acetic and butyric acid to be by-products. Miller and others have 
found lactic-acid-producing bacteria plentiful in the mouths of immune. 

Hinkins and Acree, 3 in experiments upon pure cultures of a number 
of oral bacteria in various artificial media, found lactic, butyric, 
valerianic, formic, carbonic, and hydrosulphuric acids as either 
principal or by-products of the fermentation. 

Hartzell and Henrici 4 believe that the Streptococcus brevis of 
Lingelsheim, Streptococcus viridans of Schottmuller, Streptococcus 
salivarius of Andrews and Horder and diplococcus of Poynton and 

1 Microorganisms of the Human Mouth. 

2 Ibid. 2 Dental Cosmos, 1901. 
4 Jour. Nat. Dent. Assn., May, 1917, p. 491. 



EXCITING CAUSES 249 

Paine are one and the same organism. They confirm by their 
observations Goadby, Kantorowicz and Niedergesass in finding them 
in deep layers of decalcified dentin, purely gangrenous pulp and 
chronic apical abscesses and granulomata, and also upon tooth 
surfaces, in pyorrhea pockets. They find them actually increased 
in numbers in carious conditions and that they are powerful acid 
formers. Thus they believe they have established a chain of evi- 
dence. The associate bacteria of caries are regarded as adjunct 
acid formers or saprophytes destroying the matrix. Gies and 
Kligler 1 state that in dental caries there is a great increase in the 
total number of bacteria in the mouth accompanied by a drop in 
the relative number of cocci and a marked increase in the number 
of acidific bacilli and thread-forming organisms. They refer here 
by "cocci" especially to streptococci. (Later Hartzell and Henrici 
pointed out that though relatively decreased they are numerically 
increased.) 

They arrived at the tentative opinions 1 expressed below which 
we condense: 

1. The oral flora changes from that with normal teeth and a 
specific infection occurs in which a limited number of types of bac- 
teria (perhaps three) are concerned in primary caries of enamel 
particularly a pleomorphic thread-forming organism which may 
cause attachment of the plaque and attach other forms as they do 
in the test-tube and plates, also a marked increase in the number 
of acidific bacilli which attach themselves in compact colonies to 
any surface. They name (a) Bacillus acidophilus, (b) Cladothrix 
placoides and (c) Leptothrix buccalw as prominent in carious enamel 
deposits (incipiency) ; a and b grow vigorously in each other's 
presence, are actively fermentative of common sugars and resist high 
amounts of their acidific products. They do not exclude coccus 
forms as a possible cause of acid production. 

2. There is a distinct difference between the types of bacteria 
in the early stages and those in the later periods of decay which they 
regard as modifying Howe and Hatch's discoveries of acidific bacteria 
in dentin (see page 250). 

They also give interesting data upon the effects of brushing and 
presence of food particles upon the numbers of bacteria present in 
the mouth. Two typical examples may be cited: K before brush- 
ing in the morning had 65,000,000 bacteria in each milligram of 
specimen material and 15,000,000 after brushing; H had 4,000,000 



1 Journal of Allied Societies, September, 1915, p. 313. 

2 Conveniently found in Journal of the Allied Societies, December, 1917. 



250 



DENTAL CARIES 



per milligram before a meal and 100,000,000 after the meal. This 
would correspond with a priori assumptions. 

Howe 1 in an extensive study upon the flora in cavities in the first 
and second molars of children pursued the plan of sealing the caries 
fungi in the cavities with filling without antiseptic qualities for six to 
twelve weeks (Class I) and with filling w r ith slight antiseptic qualities 
for a much shorter period (Class II) in order that extraneous bacteria 
not essentially involved in the carious process might die or be killed 
out, w r hile those more essentially associated' might thrive. The 
contents of open cavities were used as controls (Class III). In all 
three classes material was obtained from (1) the superficial, (2) the 
middle, (3) the deep layers of affected dentin and (4) from the 
apparently unaffected layer beneath. 

Fig. 257 




Bacillus acidophilus. 



Forty-eight-hour culture on glucose-agar. 
(Howe.) 



Gram stain. X 2000. 



Howe describes the microorganisms found as forming (and existing 
under) high degrees of acidity (even 14 per cent.) and states that this 
limits the number concerned to few as other organisms do not with- 
stand such acidity. He also states that they belong to the Moro- 
Tissier group and present the same morphological features as the 
bacteria of this group isolated from the intestines of nurslings. 
How r e describes the various acidific bacteria found as follows: 
"The organisms constantly found in dental caries, and belonging 
as we believe to the Moro-Tissier group because of their highly 



Dental Cosmos, October, 1917. 



EXCITING CAUSES 251 

aciduric character, we have called: Bacillus acidophilus (Moro), 
Bacillus X, Bacillus M, Bacillus Y, Bacillus bifidus. 

"Bacillus acidophilus of Moro as found in dental caries is a non- 
motile, non-pathogenic rod. When grown on agar it is short and 
thick and measures 0.75 x 2 to 3 microns. It is Gram-positive. 

"On glucose-agar the rods are longer and thinner and more dis- 
tinctly arranged in groups with the individuals showing parallelism. 
They produce turbidity of the media. They are Gram-negative. 
On blood serum the rods measure 0.1 x 1 microns. They are Gram- 
negative, grouped as in glucose-agar. 

"Bacillus acidophilus grows best anaerobically when first isolated 
by means of acid broth. In milk it clots the lower portion first. 
In peptone water it produces no indol or ammonia. In broth it 
forms a heavy sediment with some turbidity. It forms no gas in 
sugar. It is a facultative anaerobe and should be transplanted 
every ten days. It is a high acid former. Most strains ferment 
saccharose, glucose, lactose, maltose and raffinose. From 7 to 10 
c.c. of N/NaOH is required to neutralize 100 c.c. of the bouillon. 
It does not ferment lactose as readily. According to the studies we 
have made it is not as pleomorphic as has been supposed. The 
colonies are slightly raised, round, smooth, opaque and white. 

"Bacillus X is somewhat pleomorphic. It is Gram-positive on 
agar. It most frequently appears as a long chain of short, thick 
rods, 5 x 0.5 microns, the chains often showing parallelism. Under 
certain conditions the individuals are considerably longer and do 
not occur in chains. Moreover, smears of the organism often show 
only masses of long, tangled, unbroken threads, occasionally having 
one long thickened end. On glucose agar many of the individuals 
fail to retain the Gram stain. It is an anaerobe facultatively aerobic. 
It produces a high degree of acidity often requiring 14 c.c. of N/NaOH 
to neutralize 100 c.c. of the bouillon. It ferments glucose, saccharose 
and levulose, but does not ferment lactose readily. It coagulates 
milk and does not form indol or ammonia. 

"On petri dishes its colonies are transparent, round, entire, slightly 
raised. 

"Bacillus M is a small, slightly curved rod, Gram-positive on 
agar, Gram-negative on glucose agar and blood serum. In smears 
the organisms appear as bent individuals, in pairs, with concave 
sides facing each other, and in clusters, sometimes joined end to 
end and thus forming sectors of a circle. It possesses the same high, 
acid-forming properties as does Bacillus X. It grows best on glucose 
agar, on which it forms small, round, convex, cream-white to brownish 
colonies, the pigment increasing with age. 



252 



DENTAL CARIES 



"Bacillus Y is a straight or slightly curved rod with rounded and 
sometimes tapering ends. It measures from 1 to 2 microns x 0.2 of a 



Fig. 258 




Bacillus M. Forty-eight-hour culture on glucose-agar. Gram stain. X 2000. (Howe.) 

micron. The cells are arranged side by side. It is Gram-positive 
on agar and on glucose. 

Fig. 259 




Bacillus Y. Seventy-four-hour culture on glucose-agar. Gram stain. X 2000. (Howe.) 

"On blood serum it occurs in the form of rods 3 to 6 microns long, 
and as long, winding threads with a width of 0.5 of a micron. The 



EXCITING CAUSES 



253 



ends are frequently thickened. Both rods and threads are Gram- 
negative and may contain one or more Gram-positive bodies.. 

"This microorganism we have found but one or two times. We 
have reserved it for future study. 

"B. bifidus, as it appears in the carious tooth, is to be found in 
many forms. It is found frequently in its bifurcating state with 
tapering or with thickened ends, in V and Y forms, in streptococcal 
forms, as masses of Gram-negative cocci, as straight rods, in crosses 
and as a spore-former. It is Gram-positive in young cultures. It 
grows aerobically and anaerobically, although according to Kendall 
it is a strict anaerobe. Noguchi shows it to have both anaerobic 
and aerobic phases. In contradistinction to his, the bifurcating form 
of our organism grows well aerobically after adaptation to artificial 
media. The colony is raised, white, entire, butyrous." 



Fig. 260 




One form of Bacillus bifidus. 



Forty-eight-hour culture on blood-serum. 
X 2000. (Howe.) 



Gram stain. 



It is quite clear that bacteria are the exciting causes of dental caries; 
and that for their function as such they require carbohydrate material 
as food. It is probably true that in order to act, the acid-producing 
bacteria must be attached to the teeth in the form of plaques (to be 
later described), or the food and bacteria as a mass must be attached 
at some undisturbed location. 

The action of bacteria upon these substances has been studied. The 
carbohydrates introduced into the mouth as food are monosac- 
charids, disaccharids, and polysaccharids. (1) The monosaccharids 
or glucoses have the general formula CeHi20 6 , and are represented by 



254 DENTAL CARIES 

dextrose and levulose, found in seeds, fruits, roots, honey, and in 
many forms of candy, such as peanut brittle and glaces, and galac- 
tose formed from lactose or milk sugar by hydrolysis. These ferment 
directly into lactic acid without formation of gas. 

C 6 Hi 2 06 + bacterial enzyme = 2C 3 H 6 3 . 

A certain proportion of the glucose, etc., is appropriated by the 
bacteria as food. (2) Disaccharids or saccharoses have the general 
formula C12H22O11. The principal one is saccharose, found in sugar- 
cane, the sugar-beet, sugar-maple, and maize. This is inverted by 
the inverting ferment of the bacteria into glucose and levulose through 
a process of hydration : 

C12H22O11 + H 2 + bacterial enzyme = C 6 Hi 2 6 = C 6 Hi 2 6 . 

Cane sugar Water Glucose Levulose 

Two other disaccharids enter the mouth or are formed therein: 
lactose and maltose, both C12H22O11 (H 2 0). Lactose exists in milk, 
and by hydrolysis is changed by bacteria to galactose, 2C 6 Hi 2 6 , and 
then ferments like other monosaccharids. Maltose is an intermediate 
product in the formation of glucose from starch, and is produced by 
the action of ptyalin. It is readily fermentable by yeast and by 
some mouth bacteria (Goadby). (3) Polysaccharids or amyloses 
with the general formula (C 6 Hi O 5 )n. Starch, cellulose, glycogen, and 
gum. 

Starch was found by Miller 1 not to undergo direct fermentation by 
mouth bacteria — i. e., culture media containing starch, but not 
sugar, when infected by bacteria did not ferment into lactic acid 
unless ptyalin was present. When saliva was used, however, the 
acid reaction occurred, owing to the formation of glucose through the 
action of ptyalin. 

In oral fermentation starch is first changed by ptyalin to maltose 
by hydration, and the maltose to glucose. Then the bacteria change 
this to lactic acid. 

2C 6 H 10 O 6 + 2H 2 + ptyalin = C 12 H2 2 0ii(H 2 0). 
Starch. Water. Maltose. 

Erythrodextrin and achrodextrin are intermediate products. 

C 12 H 2 20ii(H 2 0) + ptyalin = 2C 6 Hi 2 6 . 
Maltose, or bacterial enzyme. 

2C 6 Hi 2 6 + bacterial enzyme = 4C 3 H 6 3 . 

According to Goadby 2 a few bacteria found in the mouth can pro- 
duce the change direct from starch to maltose and thence to acid. 
This is of no practical consequence, however, as ptyalin is always 
present in the mouth. (See Miller above.) 

Glycogen, C6H10O5, or animal starch, is fermented to glucose by liver 

1 Microorganisms of the Human Mouth. 2 Mycology of the Mouth. 



EXCITING CAUSES 255 

cell ferment. Michaels and Kirk claimed a glycogenic principle to exist 
in saliva which could be a food for the bacteria (see pages 255-269). 
Miller has demonstrated that bacteria produce acid from starches 
and sugars in about equal proportions, provided the starches are 
cooked. The cooking of starchy foods bursts the starch granules 
and renders them more adhesive to the teeth, as well as more fer- 
mentable. The following synopsis of experiments 1 made with food 
mixed with saliva in definite quantities speaks for itself: 

Duration of 
Material. experiment. Acids formed in units. 2 

Bread, starch, potato, macaroni, 

rice, corn, and other cooked 

starches 12 and 30 hours. 20 to 25 and 42 to 110 

Raw starches, potato, spinach, etc. 12 and 30 hours. 

Cane-sugar and grape-sugar . 12 and 30 hours. 17 to 20 and 37 to 41 

Meats, fish, eggs, etc. ... 12 and 30 hours. or alkaline. 

The table shows that albuminous materials and raw starches 
produce no acid and are not concerned in caries except in so far as 
meats, etc., act as culture media perpetuating bacteria, which later 
may produce an acid reaction in carbohydrate materials. 

Milk contains a carbohydrate (lactose) and often lactic acid bacilli. 
It therefore may supply both the bacilli and their food. This, 
however, has relation to caries only after plaque formation, or by 
retention of acid milk against the teeth. That such a result may 
occur has been shown by Bennett. 

Pickerill 3 tested the acid-forming powers of foodstuffs, chewed, and 
incubated for four days. The following table resulted : 

Acid units each 
neutralizing c.c. of N/5 
Food material. NaOH. 

Pastry 5.2 

White bread 4.4 

Toast 4.4 

Brown bread 3.6 

Chocolate 3.6 

Biscuit 3.5 

Apple 2.6 

Potato 2.5 

Bread and butter with jam 2.5 

Crust of bread 2.0 

Parsnip 1.7 

Orange 1.2 

Salad 1.1 

Cane-sugar 0.9 

Rice 0.9 

Meat (alkaline to acid unit N/5H2SO4) .... 4.8 alkaline 

1 Microorganisms of the Human Mouth. 

2 An acid unit equals the amount of acid necessary to neutralize an alkaline unit, i. e., 
0.1 c.c. of a 0.5 per cent, solution of potassium hydrate — e. g,, if in a quantity of acid 
material containing an unknown amount of acid, 25 of such alkaline units are neces- 
sary to neutralize the reaction, there were 25 acid units present in it. For purpose of com- 
parison the quantities of material used were 4.0 c.c. of saliva and 0.5 grams of the food, 

3 The Prevention of Dental Caries and Oral Sepsis, 



256 DENTAL CARIES 

He calls attention to the various factors of viscosity of saliva, 
natural adhesiveness of food to teeth, etc., as modifying factors in 
inception of caries. 

Dr. Harold Clark 1 has called attention to the fact that the English, 
whose teeth are much subject to caries, consume chocolate in large 
quantities. The observation of Dr. Albert King below regarding 
white bread seems partly confirmed. 

The fats may be fermented with production of fatty acids. Goadby 
has found these of no importance in relation to caries, but Miller has 
shown that the acids found in dermoid cysts, among which are fatty 
acids, can produce decalcification; as other acids were present, the 
relation of fatty acids is not quite clear. Miller asserts that fats 
deposited upon the teeth, as well as calculus retard decay, and that 
fat mixed with saliva will give an alkaline reaction 2 . 

That alkalies do not produce tooth disintegration in the mouth is 
shown by the fact that a tooth is not affected by alkaline solutions, 
which are not strong enough to injure the soft parts. 

The influence of carbohydrate diet in the production of caries is 
well shown by tables compiled by Mummery and quoted by. Miller. 3 
The races consuming a fish and meat diet almost exclusively — e. g., 
the Esquimaux — are recorded as having about 3 per cent, of caries 
in skulls examined, while those using a mixed or vegetable diet have 
from 10 to 40 per cent, of caries. A most convincing example is 
that given by Miller of two related tribes living on either side of 
the Andes, in the Argentine Republic, and Chili respectively. The 
former, a cattle breeding and meat eating tribe, were practically free 
from caries, while the latter, living on mixed foods, and consuming 
sugar, had 19 per cent, of caries. Miller and others have shown that 
millers and confectioners rapidly develop caries after engaging in 
the occupation, probably owing to the inhalation of flour and sugar 
dust. Albert B. King 4 has recorded observations upon 132 cases of 
bread eaters, finding that 87, who used bakers' bread exclusively had 
much caries, 31 who used alternately bakers' and home-made bread 
had a less prevalence, while the 14 using home-made bread exclusively 
had only six cavities in three years. The results are certainly worthy 
of attention and of further observations. I. L. Porter 5 suggests that 
the glutein in the flour used in baker's bread causes adhesion of the 
masses to the teeth. 

While the fermentation of carbohydrate food debris into acid is 
conceded to be the active exciting cause of dental caries, the modus 

1 Private communication. 2 Dental Cosmos, 1904. 

3 Microorganisms of the Human Mouth. 4 Dental Cosmos, 1905. 

3 Dental Digest, 1914, p. 147. 



EXCITING CAUSES 257 

operandi of the inception has not been satisfactorily settled. Miller 
held that as he was able to find bacterial plaques upon many sur- 
faces of teeth, even in the mouths of immunes, without caries beneath, 
the plaques had no relation to the inception of caries of enamel, but 
that the carbohydrate food collecting at favoring spots undergoes 
acid fermentation, with production of enamel decalcification, after 
which the bacteria enter. By experiments, he determined that the 
plaques rather hindered the action of acids experimentally used as a 
decalcifying agent. Black, on the other hand, claims that the bacteria 
produce a gelatinoid material and are left upon the teeth in the 
form of a plaque or zooglea mass, and that the plaque is a thin, 
transparent, slightly yellowish film, not seen without close inspection. 
(It can be stained by iodin. — Editor.) Williams found a film of 
bacteria over the decalcified area in almost all cases of superficial 
caries of enamel, and that it has sufficient resistance to permit 
grinding in situ (Figs. 276 and 277). 

Goadby frequently found on the opaque white patches of softened 
enamel, a coccus to which Williams called attention, which would 
cause a plaque deposition upon teeth suspended in its culture, and 
that when acid-producing bacteria were mixed with the coccus and a 
carbohydrate medium used, superficial decalcification of the enamel 
under the plaques was produced in from a week to ten days. 

Miller also showed that in the immune with unclean teeth, the 
putrefactive reaction was the dominant one, and that the collection, 
if persistent, could act as a protective against the access of acid- 
producing material. 

In the above data we find that the plaques are almost universal, 
even on. immune surfaces (Miller), so that their presence on a decal- 
cifying surface is probably true, as claimed by Williams. If, then, 
they are a protection against the acids produced from carbohydrate 
they should protect, but they do not. Secondly, experiments with 
formed acids are not conclusive, as they may be germicidal and 
the dead film might be a relative protection against decalcification 
by the acids. Thirdly, the bacterial films, if containing acid-pro- 
ducing bacteria, can easily take up any carbohydrate food collected 
against them, form acid from it, which they then pass to the enamel 
in a nascent state, hold it against it, and permit it to abstract the 
calcium salts, which they then pass out as lactates, etc., or allow to 
remain in situ. This latter conclusion in the main is the theory of 
Black, and while the decalcifying ability of infected carbohydrate 
food without the intervention of a definite previously formed plaque 
(but possibly by n self-formed one) is a possibility, it seems a reason- 
able conclusion to admit the activity of the plaques. Kirk has shown 
17 



25S DENTAL CARIES 

that the precipitation of mucic acid from saliva rich in mucin content, 
by lactic acid produced by lactic acid bacilli, plays a part in the 
development of the plaques, or by binding the bacteria together 
creates a bacterial plaque. Von Beiist 1 has shown that within three 
hours, a mucinous deposit containing many colonies of bacteria which 
rapidly increase in size, may be formed. He attributes to bacteria, 
a large share in the formation of calculus which is the theme of his 
paper, but it also throws light on caries plaques. 

The frequent disturbance of the plaques by monthly cleansings 
(prophylaxis), also prevents dental caries in large degree, so that they 
must have some relation to the inception, though it is only fair to 
state that a constant warfare against any species of bacteria doubtless 
vastly reduces their number in the mouth. 

Noyes 2 claims that in well-cared-for mouths the confinement of 
acid under the plaques is great, while in uncared-for mouths, though 
much acid is formed, it may be dissipated in the saliva and the teeth 
not be much attacked. This argument, however, does not take into 
consideration the idea of Miller, that stagnant materials take on a 
putrefactive reaction after the acid production is exhausted (see 
p. 271). 

The Predisposing Causes of Caries. — The causes of the predis- 
position to caries are local and general. 

Local Predisposing Causes. — So invariably does caries begin in 
sulci or pits upon approximal surfaces, about defective fillings, and 
upon unclean surfaces, that faults of form or retentive nature of 
approximation, defects, and faulty position of the teeth must bear a 
relation to the difficulty of keeping the parts free from accumulations 
of bacteria and carbohydrates. 

These local predisposing causes, as they are called, are simply 
conditions favoring the formation of the bacterial plaques upon the 
teeth and the retention of carbohydrate food. 

Lack of Oral Hygiene. — This is perhaps the most frequent local 
predisponent of caries. It is, in fact, a factor in the exciting cause 
and its reverse is prophylaxis. Most people either can not or will 
not cleanse the teeth thoroughly, hence their lack of care predisposes 
them to caries. It may not occur, but is liable to do so. Otherwise 
lack of hygiene means the presence of microbic plaques and carbo- 
hydrate food, and these are exciting causes of caries. 

Faults of Form. — Deep pits or sulci in the occlusal surfaces of 
bicuspids or the occlusal or buccal surfaces of molars, or in the lingual 
surfaces of incisors, and occasionally cuspids, or pits upon the cusps 

» Items of Interest June, 1912. 2 Ibid., 1909. p. 750. 



PREDISPOSING CAUSES 259 

of bicuspids or molars, or in other unusual situations, are not sub- 
jected to a cleansing friction, and so permit bacteria to form plaques 
in these locations (Figs. 262 to 275). 

The nature of the approximal contact has to do with the inception 
of caries. Teeth are seen in which the approximal surfaces are well 
rounded and their buccal and lingual angles free from approximation. 
Such teeth are usually relatively narrow at their cervices, so that 
these also recede well from the line of contact. A V-shaped space 
is formed, which the gum festoon normally nearly fills. Such per- 
fection of contour is also, as a rule, associated with a perfect organi- 
zation of the enamel structure, in virtue of which the surface is 
smooth. While such teeth may decay approximally, there is much 
less tendency to caries (Figs. 278 and 284). 

Opposed to this, approximations exist of a broad nature. Broad 
approximations are very common, and not infrequently are asso- 
ciated with a certain degree of enamel opacity and an unevenness 
of enamel surface plainly visible to the naked eye (see page 148). 

The fluid exuded by the gum is normally alkaline in character, 
and probably neutralizes the products of acid fermentation. Mendel 1 
has shown that the gingival exudate contains large numbers of phago- 
cytes. In view of this fact, the first-mentioned form of contact evi- 
dently affords more of this immunizing principle. The extension of 
cavity margins beneath the gum has been strongly indicated by 
experience as good practice, and probably is explainable upon this 
ground and by phagocytosis as there is evidence that the gum has 
some such action upon metal placed beneath it, as it is noted that 
when unclean gold crowns are removed the portion extending beneath 
the gum is usually quite clean. 

With the narrow approximations, saliva is readily forced between 
the teeth and neutralizes the acids formed, or washes away soluble 
carbohydrates, the food for the bacteria. With the broad approxima- 
tions such a result is less likely to occur. 

Stagnant saliva retaining carbohydrates, probably will develop an 
acid reaction. (Miller.) 

A depressed approximal surface may decay, but frequently does 
not. An acquired fault of form requires notice. 

Anatomically, the gum covers the cementum and the enamel 
margin. When recession of the gum occurs, the cementum is left 
exposed and food debris accumulates at the angle formed by it with 
the gum. Owing to the cementum being less smooth than enamel, 
microbic plaques readily collect, hence decay of the cementum 

1 Anali di Stomatologia, 1917; See Cosmos, 1917, p. 760. 



260 DENTAL CARIES 

frequently occurs, and is apt to progress rapidly, owing to the 
natural low percentage of inorganic matter (Figs. 268, 302, and 303). 

Wachsler 1 has called attention to symmetry in caries, i. e., in like 
locations on opposite sides of the mouth. He attributes this to irri- 
tation of trophic centers through a reflex, while Horrowitz 2 antago- 
nizes this view, considering it due to symmetric local predisposing 
causes (malformations or peculiarities of structure form approxima- 
tion, etc.) inviting like inceptions. 

Arrangement and Position of the Teeth. — The overlapping 
of one tooth upon another creates a form' of contact, producing a 
tendency to decay at that point. Angle 3 claims to have observed a 
comparative freedom from caries of very irregular teeth (Fig. 275). 

The presence of a supernumerary third molar, lying at the buccal 
side of the interdental space, between the second and third upper 
molar, or an inlocked bicuspid, very frequently causes approximal 
caries at the contact points. The upper third and lower third molars 
frequently stand in bad relation to the cheek or the gum. 

Food collects upon their buccal surfaces, or they are not subjected 
to the friction of the tooth-brush, and decalcification of a broad area 
of a buccal surface frequently results. 

Defects about Fillings. — Under the caption of Recurrence of 
Caries, will be found a list of the causes which perpetuate caries about 
fillings. Defectively cemented bands are also a cause. I believe 
the abundance of these and a lack of oral hygiene to be, in a large 
degree, the measure of a tendency to persistent caries. A patient 
has a large number of cavities due to a period of negligence, with 
consequent intensity of oral fermentation. If these are obliterated 
in the best manner with physically perfect fillings, and oral hygiene 
be exact, the tendency to caries is largely obliterated. If, on the 
other hand, a large number of even slightly defective fillings are 
made, not only is recurrent caries induced, but the caries ferment is 
continuously active, and exact oral hygiene is an impossibility. The 
number of cleansings a day is no guarantee of perfect hygiene, even 
with perfect teeth, as nothing is more common than to see unclean 
embrasures easily taking the stain of tincture of iodin even in the 
anterior part of the mouth (in less degree than shown in Fig. 261). 
Unquestionably, food debris may even be swept into the interdental 
spaces by brushing alone. Miller 4 has shown that a mixture of bread 
and saliva may become decidedly acid in one hour, and superficially 
decalcify sections of dentin in five hours. With this going on, day 
after day, in cases of soluble teeth and without other aid than 

1 Dental Cosmos, March, 1915. 2 Ibid., June, 1915. 

3 Ibid., 1903. 4 Ibid., 1905. 



PREDISPOSING CAUSES 261 

brushing, and often this not thoroughly done, the persistence of 
decay is not surprising. This, however, does not prove the absence 
of systemic susceptibility or immunity, as an added cause of caries 
or its absence. A condition similar to a defect about a filling, is 
that of the presence of an orthodontic appliance which may afford 
convenient nooks for caries fungi, and food. In the use of base 
metal wires about teeth for pyorrhea, the wire either has some anti- 
septic, action probably due to the contained copper, or the pyorrhetic 
condition itself furnishes an alkaline element. In such case caries 
frequently does not occur. 

Fig. 261 




Caries of enamel about the cervices of many teeth, due to tenacious films collected 
upon them; at first probably neglected, later impossible to cleanse with brush alone. 
(Model by W. A. Capon.) Fairly clean teeth stained with iodin present such an appear- 
ance. (See prophylaxis.) 



Structure. — While the structure of the enamel has no relation to 
the inception of caries, that is, teeth of poor structure may not 
decay, a roughness of the enamel surface, which often accompanies 
teeth of opaque appearance, may act as a favoring condition, 
and after inception of caries, inferior structure and possibly the 
presence of Caush's tubes may permit more rapid disintegration. 
(See p. 145.) * An interesting examination of 16,000 mouths, made in 
Sweden by Forberg (Stockholm), and others by Rose in Baden and 
Thuringia seems to show that there is a relation between the color 
(structure) of teeth and the presence of caries, the following averages 

1 This statement now made in two editions has been further experimentally con- 
firmed by Pickerill (The Prevention of Dental Caries and Oral Sepsis, 2nd Ed.), who 
has shown by rubbing graphite upon the surface, what he terms "imbrication lines," 
which are associated with "calcarine" fissures in some teeth. Those teeth which 
contain many of the lines and fissures are termed "malacotic, " while those but 
slightly imbricated are termed "sclerotic." By test, "malacotic" teeth were found 
more soluble in lactic acid solutions than the sclerotic (Ibid., p. 129). A similar 
result was obtained with hydrochloric acid. Malacotic and sclerotic teeth were both 
but little affected after insertion into an orange for a week but the malacotic were more 
affected (Ibid., p. 130): This fact is of importance in prophylaxis (which see). Carbon 
dioxid in strong solution was found to have no effect upon teeth (Ibid, p. 133). 



202 DENTAL CARIES 

of all ages being observed: White teeth, 14.3 per cent, of caries; 
yellowish-white, 16.4 per cent.; yellow, 20 per cent.; grayish blue, 
24.3 per cent. 

According to these observers, 1 in the regions in which the water 
was rich in calcium salts the individuals examined had the yellowish- 
white teeth. 

Yamagishe 2 observes that he has found clinically considerably more 
decay in the teeth of patients with light hair and that extracted teeth 
from light haired patients decalcify more in dilute hydrochloric acid 
than the extracted teeth of dark haired patients. The "brownin" 
of Black may have some relation to this (see page 156). 

Gautier 3 has found that in young pigs, deficient osseous development 
corresponded exactly to the lack of calcium salts in their drinking 
water. 

McKay 4 in investigating mottled enamel found that poor quality 
of enamel occurs in localities the water of which shows highest lime 
content and equally poor enamel in localities having water of low- 
calcium content. 

Black 5 made analyses of so-called hard and soft teeth, and deduced 
from them the opinion that the hardness and softness of teeth have 
nothing to do with the inception of caries. 

Touching this point, Black 6 instances the case of a man whose 
enamel had always been chalky and as easily cut as a slate-pencil, 
yet who had little caries of the teeth. That some teeth of apparently 
poor structure and defective form do not decay is also a fact of 
common observation, but, as a rule, they go together. 

Other Local Predisposing Causes. — Acids taken in excess into 
the mouth may act as predisponents by causing a roughness of the 
enamel, which invites the formation of the bacterial plaques. A 
course of tincture of ferric chlorid has a bad reputation in this con- 
nection. In the cases observed by the editor, the hydrochloric acid 
in the tincture seemed to have formed roughnesses between the 
teeth, and many large cavities of not unusual form were later pro- 
duced and evidently due to the carious process. Weld, 7 in a series 
of experiments to determine the action of ferric chlorid, found that 
the pure tincture had little effect, while in the dilution of 1 : 5 in water 
it had much; destroying the entire enamel in twenty-four hours. 
Head's observations on the effect of dilute acids are in general accord 
with this principle (see page 216). This fact indicates the prompt 

1 Dental Cosmos, 1911. 2 Ibid., 1917, p. 1008. 

3 L'Odontologie, October, 1910. See Cosmos, 1911, p. 242. 
« Dental Cosmos, July, 1916, p. 792. 6 Ibid., 1898. « Ibid. 

7 Quoted by Prentiss, Dental Cosmos, September, 1912, p. 1006. 



PREDISPOSING CAUSES 263 

local use of an alkali after a dose. (See Prophylaxis of Caries.) 
Howe 1 claims that iron, whether as chlorid or carbonate, taken in 
capsules, returns to the salivary gland for excretion as ferric chlorid 
and may exert injurious effects. 

Morjenstern 2 describes experiments that show that acid iron waters 
or tinctures have a decalcifying action, ferrous iodid and ferric 
chlorid being particularly injurious, while reduced iron, saccharated 
solution of iron, and albuminate of iron produced no ill effects either 
local or through systemic action. 

The acid vomitus of pregnancy and seasickness have an analogous 
effect. It is not likely, however, that during a transatlantic voyage 
large cavities can develop. The probable explanation of the presence 
of such cavities directly after the voyage is that they existed before 
the voyage was begun. Cavities are frequently left or overlooked. 
(See Prophylaxis of Caries.) Since the advent of medication by 
lactic acid preparations and those containing lactic acid bacilli, such 
as sour milk, analogous effects have been observed, and therefore the 
mouth should be washed out with alkaline antiseptics after such 
remedies are taken. 3 4 

Miller found that the saliva has no antiseptic quality as a whole 
and contains no antiseptic substance, and though he found the saliva 
of immunes to develop a little less acid than that of highly susceptible 
individuals, the difference was not constant and not sufficient to 
account for the marked difference in susceptibility. Miller found that 
carbohydrate foodstuffs mixed with an alkaline saliva became even 
more acid than when the reaction of the saliva was intensely acid 
and the chance for caries was about the same with either reaction 
at the start. Goadby 5 calls attention to the demonstration of Savarelli 
that saliva is germicidal for small quantities of bacteria but loses 
its property with large quantities. This may have some bearing 
on caries prevention. 

Under conditions of oral irritation, such as catarrhal stomatitis, 
or even the presence of many cavities of decay, a stringy, mucinous 
condition of the saliva may result. This may be due to a partial 
coagulation of the mucin by the acid present in the mouth, and the 
coagulum may entangle food masses and cause their adherence to 
the teeth. 

1 Dental Cosmos, January, 1913, p. 39. 

* Therapeutische Monatshefte, 1908. 3 Vanel, Dental Cosmos, 1904, p. 694. 

4 1 had a patient with an enormous amount of caries. He had used buttermilk daily 
for a year or two. I asked him to stop but he continued. To my surprise he has but 
little new caries twelve months after completion of his large line of work. This upset 
is as puzzling as the case of the man who forms calculus freely and rapidly though prac- 
tically starving because of inability to swallow. (See Calculus.) 

* Mycology of the Mouth. 



264 DENTAL CARIES 

Lack of Saliva of Alkaline Potential. — Pickerill, 1 in exhaustive 
experiments, shows that a continuous flow of saliva may be reflexly 
excited by foodstuffs having taste and flavor, and especially by 
organic acids of fruit, and argues that such alkaline saliva by flowing 
over teeth neutralizes any acid formed by fermentation. Per contra, 
its absence may be a cause of caries. The argument looks rational, 
but Pickerill has not given any experiments upon susceptible in- 
dividuals to prove his case. Marshall, 2 as the results of experiments 
to show a relation between carious teeth and the composition of the 
saliva, offers the following deduction: "The normal resting saliva 
of persons with carious teeth is characterized by (1) a relatively high 
neutralizing power and therefore presumably, (2) a high content of 
diffusible substances, (3) a low content of proteins." He states that 
the neutralizing power of resting saliva is supernormal while that of 
saliva activated by chewing paraffin is subnormal. He states also 
that, on the contrary, activation of an immune to caries produces a 
saliva of greater neutralizing power than that of the normal resting 
saliva, and having a considerably lower protein content and higher 
content of inorganic salts. 

Howe and Gies, separately working in this field, claim that there is 
no constant relation between the neutralizing power of resting and 
activated saliva and the incidence of dental caries while admitting its 
neutralizing power. That is, no salivary index is established, as 
claimed by Marshall. 

Very dry mouths (xerostomia) have a viscid, tenacious saliva, and 
usually cervical caries is present. Some individuals are greatly incon- 
venienced and may have to frequently moisten the mouth to obtain 
comfort. 

Pickerill 3 views a hyperdevelopment of the nervous system as liable 
to lead to salivary depression through cerebral stimulation and states 
that exacerbations of caries occurs in certain mouths during periods 
of nervous stress. 

The contention of Lohmann that the carbohydrate element in 
mucin was the cause of caries, Miller examined experimentally and 
found it untenable, but that the explanation here given of its entan- 
gling action is the probable one. He states that very small amounts 
of lactic acid precipitate the mucin and thus enable the bacteria to 
become fixed to the teeth as plaques. 

Miller has noted that some immunes have had exceedingly ropy 
saliva which could be drawn out into long threads, while much 

1 The Prevention of Caries and Oral Sepsis, 2d Ed. 

2 Journal of Nat. Dental Assn., 1917, p. 782. 

3 British Dental Journal, 1915, and Cosmos, June 15, p. 715. 



PREDISPOSING CAUSES 265 

caries was noted in the mouths of some almost absolutely free from 
mucus. 

Miller could find no antiseptic quality in the saliva, nor any prin- 
ciple corresponding to alexin, and found that bacteria developed in 
the saliva of immunes almost as readily as in that of those susceptible 
to caries. 

He also pointed out that the mucus may readily undergo putre- 
factive fermentation with alkaline reaction, and, again, the carbo- 
hydrates entangled in it will ferment with acid reaction, causing any 
caries which might be attributable to mucin fermentation. Gies 1 
has shown that salivary mucin forms viscid films on the teeth, which 
tend to thicken by accretion and in which millions of bacteria 
multiply, particularly at night, when the secretions are strongest. 

It is possible that the secretion from the gum may in some cases 
be acid and favor the production of caries by decalcifying the enamel 
about the cervix (Fig. 261). 

Cook has shown that glycogenic infiltration of the oral mucous 
membrane may be produced by the use of irritant or astringent 
washes, which may possibly permit a change of this substance by 
bacteria into acid about the necks of teeth, accounting for a certain 
form of cervical decay long thought to be due to an acid mucus. 

These observations, together with the foregoing data, regarding 
the inception of caries, point to the now conceded conclusion that 
the caries of teeth is entirely due to the environment of the teeth, 
and in no sense does it arise from within the tooth, and that in so 
far as the cause is active, it is a question of the localization of the 
exciting cause or its factors on the one hand, and the solubility of 
the teeth on the other; and that no amount of cause is sufficient to 
produce it, unless permitted to exert its effect upon special points 
upon the teeth; in other words, it requires localization and time to 
act, though it may in some cases be broadly localized. 

Systemic Predisposing Causes. — Some individuals seem to 
suffer much from caries; others in less degree. In either case, periods 
of immunity or comparative immunity may be established, and may 
be again followed by a period of susceptibility and a succeeding 
immunity. 

Black has shown that caries fungi are always present in the mouth, 
but do not always form the plaques. Cases also exist in which caries 
has begun during some period of susceptibility and a number of new 
cavities have been started. Later a period of immunity has followed 
and the cavities have not progressed. 

1 Journal of the Allied Societies, June, 1912. 




266 DENTAL CARIES 

These facts point to the conclusion that a period of caries is due to 
one of the following causes: (1) The bacteria in the plaques or food 
are of an active acid-producing kind (or in immunity they are not of 
acid-producing variety) or (2) that some systemic condition changes 
the constitution of the oral fluids, permitting the formation of the 
microbic plaques upon the teeth, or (3) increases the fermentation 
by supplying some element nutritive to bacteria or (4) depriving it 
of some element inhibiting the growth of bacteria. 

So far as classed, systemic conditions influencing susceptibility 
and immunity may be placed under the four headings: Heredity, 
Prenatal and Postnatal Influences, Age, and Bodily Condition. 

Heredity. — Black 1 records observations on certain families as 
showing a tendency to caries of certain teeth at a given age, or in 
certain positions upon the teeth, e. g., occlusal pits. In certain cases 
the hereditary tendency persists. This tendency must be due either 
to an inherited cell physiology, or diet tendency influencing the oral 
fluid, or to transmitted faults of form or, possibly, of structure of 
the teeth. 

Prenatal and Postnatal Influences. — It is quite probable that 
the systemic condition of the mother during gestation may pro- 
foundly modify the anatomicophysiological condition of the body 
cells of the child; nutritional processes may suffer and the postnatal 
tooth development proceed irregularly, structure being affected; 
moreover, the altered biochemical function of the cells may stand 
in close relation to the constitution of the oral fluids, and these in 
turn may favor the development of caries fungi. If, therefore, the 
mother is not properly nourished, the teeth may not be well con- 
structed, especially if lime be lacking in her food. The same line of 
argument may be applied to bottle feeding of recently born infants, 
or to other conditions profoundly affecting general nutrition. In 
this connection, the absence of the influence of the internal secretion 
containing hormones which should be transmitted from mother to 
child by way of the milk, may in the future be shown to have a 
bearing upon cell development and consequently upon the product 
(as the enamel). 

In an examination of school children, Th. Frick 2 (Zurich) found a 
much greater percentage of decay in children that had been bottle- 
fed at between three and six months of age. He performed an experi- 
ment on a litter of six dogs, feeding three on cows' milk and bouillon; 
one of them died, and the others had poorly developed teeth. The 
controls were normal. 

1 Dental Cosmos, 1904. 2 Ibid., 1901. 



PREDISPOSING CAUSES 267 

Breast feeding of infant is important, therefore inasmuch as cows' 
milk cannot be modified to exactly meet the demands, though one 
often may discover a susceptible who was artificially fed, yet one also 
finds breast-fed individuals with poor teeth. Rickets, which is a dis- 
ease due to improper diet, may in young infants have a like effect 
upon tooth structure. 1 

Forberg and Rose 2 have shown that the individuals who drink 
water rich in calcium salts have a smaller percentage of caries than 
those drinking soft waters. Ferrier has observed a coincidence of 
caries and the drinking of boiled water which had been deprived of 
calcium carbonate. Whether this effect is due to a better develop- 
ment of tooth structure or is a post-developmental effect is not stated 
in either case. The point brought up by Head, 3 who has shown 
the apparent rehardening of teeth in saliva after partial decalcifica- 
tion by a weak acid, opens up the question here as to whether the use 
of calcareous waters after tooth eruption can increase the density of 
enamel or, more accurately, fill up interstices in malacotic teeth. 
Enamel can be dried, why then not infiltrated by calcareous solutions ? 
The question cannot now be answered, though Gies 4 has shown " that 
water passes freely back and forth through all parts including the 
enamel of fully developed natural extracted teeth," and "that simple 
mineral salts and common organic substances such as cane-sugar 
similarly diffuse." Another view might be that some of the calcium 
salts in drinking water come back to the saliva eventually, and if 
abundant may neutralize the acidity in plaques, through their alka- 
linity, by combining with the acids formed. 

Age. — That the age has an influence upon caries was noted by 
Flagg. He recorded the ages from five to eight, twelve to twenty, 
thirty to thirty-five, forty-five to fifty, sixty to sixty-five years, and 
senility as periods of decay, while the intervening periods were 
intervals of comparative exemption. 

Black has noted that caries is a disease of youth, most intense 
before adult age, at which time immunity is established, provided the 
teeth have been well and promptly filled and the mouth otherwise 
cared for. In view of this fact, he aimed at establishing this immunity 
by close attention to the teeth during youth. 

He records fluctuations in susceptibility not unlike those recorded 
by Flagg, and also points out that some persons pass through the 
ordinary periods of susceptibility and first develop caries in middle 

1 Gies and his collaborators relate interesting though not conclusive experiments on 
this subject in Journal of Allied Societies, March, 1916. 

2 Dental Cosmos; 1899. 3 See p. 216. 
4 See Dental Cosmos, December, 1917, p. 1240. 



268 DENTAL CARIES 

age. In old age, general recession of the gum is common, and in the 
conditions of debility associated with old age, much caries of cemen- 
tum occurs. The patients are often either unwilling or unable to 
keep the cementum cleansed. 

Repeated examinations of the mouths of school-children show a 
deplorable amount of caries which may, perhaps, be attributable to 
several causes, such as the induction of a lessened systemic resistance 
due to confinement, study, etc., and also to the inhalation of vitiated 
air, which presumably also contains acid-producing bacteria. More- 
over, bacteria of caries may be directly transmitted by kissing, 
common use of drinking cups, pencils, etc. Much neglect exists. 

Michaels, 1 of Paris, has observed that "the saliva of adolescence 
contains a dextrinic principle (glycogen) susceptible of fermentation 
under the influence of ptyalin in the presence of earthy salts. Lactic 
acid is formed/' 

Bodily Condition. — It is a matter of observation that such con- 
ditions as pregnancy, typhoid fever, anemia, leukemia, diabetes, 
dyspepsia, nervous exhaustion, and debility are frequently accom- 
panied by or followed by a development of cavities of decay, but 
whether the diseases themselves or a coincident lack of oral hygiene 
act to permit the formation of the microbic plaques has not clearly 
been made out. If oral and dental prophylaxis be practised during 
these conditions and convalescence therefrom, the production of 
cavities is much limited, but this does not prove anything. 2 The same 
is true of pregnancy, which introduces an exciting cause (the vom- 
itus), and of glycosuria, which may introduce glucose, or a ferment- 
able substance as claimed by Michael, 3 according to whom it takes 
a red coloration with Nessler's reagent, which passes into a grayish 
blue. Black contends that periods of susceptibility are noted both 
in apparent good and ill health. That apparent health may really 
not be true health is a matter that must be considered. 

This bodily condition is seemingly the key to any change which 
can occur in saliva, or mucus, or oral phagocytosis, to one of which 
must be attributed any possible systemic effect upon caries bacteria, 
which can aid or inhibit their growth or localization. It matters very 
little whether the bodily condition is due to heredity as a general 
modification of cell physiology, to age, or some period of stress, as. 



1 Sialosemeiology. See Dental Cosmos, 1900. 

2 A caries susceptible was treated after pregnancy and during lactation for many 
cavities. The value of prophylaxis was finally so impressed upon her that she practised 
it properly. Since then she has had typhoid fever, but no increase in caries; which 
amounts only to about one small cavity a year; her daughter, aged nine years, has been 
treated by the mother and has never needed attention beyond occasional examination. 

3 Quoted by Kirk, see Dental Cosmos, January, 1914, p. 5. 



PREDISPOSING CAUSES 269 

the "change" of the teeth, puberty, growth during adolescence, 
diet, business or family anxieties, the degenerative tendencies of 
advancing age, or to some more acute systemic condition, as typhoid 
fever, diabetes, etc., except in so far as these conditions may intro- 
duce into the oral fluid a substance which may act either (1) as a 
direct decalcifying agent (an acid) or (2) as an indirect decalcifying 
agent, by furnishing a food material for the bacteria from which they 
may manufacture acid (a carbohydrate), or (3) furnish a substance 
in the saliva which may glue the germs to the teeth, or (4) take from 
the saliva some substance which normally inhibits plaque formation. 

It was shown under the caption of Erosion, that a very weak acid 
may decalcify more rapidly than a stronger solution, and it has 
been noted that in systemic conditions inducing general acidosis 
(as chronic nephritis or diabetes) there is a tendency to deep decalci- 
fication of cervices of teeth, beginning particularly upon the cemen- 
tum. While by no means proved not due largely to fermentation of 
carbohydrate food by bacterial plaques, as a result of defective 
hygiene, there is, nevertheless, a strong suspicion that the acidosis 
expressed as acidity of saliva has produced the decalcification. There 
is also a probable reduction in the amount of normal sodium phos- 
phates as the result of the general acidosis, and this also found in 
the saliva reduces the controlling quality, which Head has shown 
to exist when a certain percentage of basic sodium phosphate is 
present in solutions having an acid reaction. (See page 216.) 

Michaels 1 states that the constitution of the saliva changes with 
the establishment of various diatheses, and that a physiological 
saliva with the biochemical principles in a state of equilibrium is 
probably very rare. He states that the most active dental caries is 
found in the mouths of hypo-acid individuals, in whom saline chlorids 
predominate over the acid elements of metabolic waste, reducing the 
acidity of body fluids below normal, and inducing a lessened resist- 
ance to development of infective causes, and that caries is least active 
in the hyperacid individuals, in whom sulphocyanid of potassium is 
more abundant in the saliva. He has also claimed to have found 
glycogen in the saliva of adolescents. 

Kirk 2 claims that in the caries susceptible, the saliva is alkaline to 
litmus, though it may be acid to other reagents (may be ampho- 
teric). That the alkalinity keeps the mucinous elements in solution, 
and at the same time a substance analogous to glycogen and fer- 
mentable by caries bacteria is transuded by the salivary glands, 
which furnishes the. bacteria their pabulum after their fixation in 

1 Dental Cosmos, December, 1900. 

2 Items of Interest, July, 1902, p. 546. 



270 DENTAL CARIES 

plaques upon the teeth. He regards this glycogenic principle in the 
saliva as due to carbohydrate diet in excess of the body's needs 
and its capability of storage as fat; that it enters the blood after 
the glycogenic function of the liver has been exerted, increases 
its sugar content beyond the normal of 0.001 per cent. 1 (Prinz 
states it as 0.06 to 0.11 present) by test Kirk 2 has claimed sugar in 
the saliva of diabetics, but Prinz 3 in his tests in active diabetes denies 
its presence in normal or pathologic saliva. He regards the varia- 
tions in susceptibility as due to variations in carbohydrate diet. 

Kirk has succeeded in altering viscid saliva to a more limpid condi- 
tion, by reducing the ratio of carbohydrate to proteid diet, first cutting 
out carbohydrates almost altogether, then adding them gradually to 
the diet. He cites observations upon asylum children kept upon 
well-balanced rations, as having large numbers of arrested caries. 4 

In a recent article, 5 the possible influence of the hypophysis 
cerebri upon the presence of an excess of sugar in the blood and of 
this as a possible explanation of caries susceptibility, is treated of 
by Kirk, who, however, disclaims any definite finality at present. 

Pickerill argues that as glycogen is rapidly converted into maltose 
and iso-maltose by ptyalin, glycogen and ptyalin should be chemi- 
cally incompatible. He states that in his examination of the saliva 
of diabetics and those suffering from other disease, no sign of glucose 
has been present. Gies' 6 tests for glucose in saliva and glycogen in 
the mucin were negative. Taking the evidence glucose, in saliva even 
in diabetes is not proved. (See also Lohmann page 264.) 

Gies, 7 conducting elaborate experiments concerning the inhibitory 
effect of potassium sulphocyanate upon plaque formation, concludes 
that it is an excretion having no determined bearing upon caries. 
Both he and Howe 8 found experimentally that it did not inhibit 
bacterial growth in cultures. Howe considers it increases the growth. 
Pickerill 9 seems to have found a different conclusion, but in an inves- 
tigation of fifty Maori immune children found the sulphocyanate 
extremely low and in 22 per cent, absent. The Committee on Scientific 
Research of the New York State Dental Society furnish the following 
tests for it: 

Take 2 c.c. of saliva, to which add 2 c.c. of distilled water, and 
shake thoroughly together. Add 5 drops of iron perchlorid, and 
shake again. 

1 See Article on Caries in Fones's Mouth Hygiene, p. 203. 

2 Dental Cosmos, January, 1914. 3 Ibid., April, 1918, p. 292. 

4 Dental Brief, 1907. 5 Dental Cosmos, January, 1914. 

• Ibid., 1914, p. 408. 7 Ibid., 913. 

8 The Journal of The Allied Societies, June, 1912. 

9 The Prevention of Dental Caries and Oral Sepsis. 



PREDISPOSING CAUSES 271 

The presence of sulphocyanate naturally in the saliva is determined 
by the color. 

A straw color indicates little or none. A brick color indicates a 
sufficiency. A wine color indicates abundance. 

The Committee on Scientific Research, of the National Dental 
Association, 1 have devised a colorimetric scale which consists of two 
tubes. In tube A, 1 c.c. of saliva is placed. In tube B, 1 c.c. of a 1 to 
2000 solution of sulphocyanate of ammonia. To each, add 2 drops 
of a 5 per cent, ferric chlorid solution from the same pipette. Add 
distilled water; to be in definite quantities until the color matches 
that of the saliva. Calculation of the dilution of the standard 
solution will give the amount of sulphocyanate in the saliva. The 
observations are introduced, that others may continue the line of 
thought. 

The use of potassium or sodium sulphocyanate internally in { 
to 1 grain doses, in tablet form, has been recommended as a prophy- 
lactic, but while some claim value it is quite likely that other means, 
such as oral prophylaxis conjoined with it, have had much to do with 
lessened caries and hypersensitivity of dentin, as claimed. 

Potassium sulphocyanate is described as a nerve tonic, safe in even 
10 grain doses. It must not be confused with potassium cyanate, which 
is a virulent poison. 

Lohmann reports success in susceptibles from the use of rhodalzia, 
a combination of albumin with 19.4 per cent, of sulfocyanic acid in 
place of other preparation. 

Black 2 believes that the condition of the system alters the oral 
fluid, so as to permit the bacteria in it to produce a gelatinoid material 
as a by-product, in one case and not to produce it in another, and 
that when produced, plaques adhere to the teeth in sheltered spots, 
while when not produced no plaques adhere, though a general acidity 
of the oral fluids may be produced. 

Miller, 3 some years ago, pointed out that filthy mouths often do 
not contain carious teeth. He offered the rational explanation that 
the unchanged adhering collections, once their acid-producing capa- 
city is destroyed, can even act as a protection in so far as caries is 
concerned. In experiments on artificial production of caries, Miller 
found that the pabulum of the bacteria needed constant change, 
otherwise putrefaction resulted and decay ceased. The fact that 
fairly cared-for mouths often contain carious teeth is rather an 
argument in favor of the local etiology of caries, as teeth unbrushed 

1 Dental Cosmos, 1908, p. 1365. 

2 Dental Digest, 1907. 

3 Lecture at the University of Pennsylvania. 




272 DENTAL CARIES 

after a meal, or, rather, not thoroughly cleansed, as is the rule in a 
vast majority of mouths, contain every necessary factor of caries, 
including a renewal of fresh carbohydrate food for the bacteria. 
As prophylaxis becomes more accurate, mouths usually pass into 
a condition suggesting a condition of immunity. It would seem, 
therefore, that unless some other factor of prophylaxis can be intro- 
duced, the mouth should either be thoroughly cleansed or not at all, 
so far as caries is concerned. As bearing on this point, a patient of the 
writer, about forty-five years of age, was for years an immune in his 
hands and would not permit his teeth to be cleansed. He was finally 
persuaded to allow it, and he departed from his immunity. His wife 
is the patient referred to on page 268. 

The whole subject of susceptibility and immunity to caries is 
yet obscure, but the accurate experimental studies are seemingly 
gradually approaching the conclusion that caries is a question of the 
presence or absence of a specific local cause. 



CHAPTER IX 

DENTAL CARIES: PATHOLOGY, MORBID ANATOMY, 
AND CLINICAL HISTORY. 

PATHOLOGY AND MORBID ANATOMY. 

It is a fact of common observation that caries begins only at 
spots protected from friction or uncleansed. These are in order of 
frequency: (1) Pits, grooves, and fissures in the enamel; (2) approxi- 
mal surfaces just above the contact point; (3) smooth surfaces which 



Fig. 262 



Fig. 263 



Fig. 264 




Fig. 266 





Fig. 267 



# 




Fig. 268 




Fig. 265 




Fig. 269 




Fig. 270 




Fig. 273 



Fig. 271 



Fig. 272 




Fig. 274 





Fig. 275 




from any cause are habitually unclean; (4) necks of the teeth at or 
near the junction of the cementum and enamel (Black) (Figs. 262 
to 275). 

In these situations Williams has demonstrated the fact that the 
oral bacteria, protected from friction, attach themselves to the 
18 (273) 



274 



DENTAL CARIES 



enamel, forming microbic plaques which are sufficiently adherent 
to permit their retention during the grinding of the specimen for 
microscopic examination. (See Figs. 276, 277, and 278.) Carbo- 
hydrate food debris lodges at the points at which retention is favored, 
and either ferments directly against the enamel, or through the 
medium of the microbic plaque. 

The bacteria in the plaque require food and obtain it from the 
carbohydrate and albuminous materials which come in contact with 
them. From the carbohydrates lactic acid is produced as a waste 

Fig. 276 




Section of normal human enamel, showing thick, felt-like mass of microorganisms 
slightly raised from the surface of the tissue, by pressure of the cover-glass in mounting. 
X 250. (Williams.) 



product. (See Chapter VIII.) Williams states that it is "highly 
improbable that the enamel is affected, except in rare and special 
instances by any other acid than that which is being excreted by the 
bacteria at the very point at which they are attached to the enamel.' ' 

This thick mass of fungi also prevents the excreted acid from 
being washed away, so that it exerts its full chemical power upon 
calcific tissue. 

The lactic acid produced attacks the inorganic matter of the 



PATHOLOGY AND MORBID ANATOMY 



275 



enamel, following first the interprismatic cement substance between 
the prisms, later dissolving the transverse cement substance between 
the globules. The effect is to produce an irregular, roughened sur- 
face of the enamel and to bring into view the structure of the rods 
(Fig. 277). 

Fig. 277 





y 



Microorganisms of caries attached to enamel on approximal surface of tooth. 

(Williams.) 



The gradual loss of cement substance unbinds the enamel globules, 
which are in turn dissolved and washed away, leaving a depression 
or cavity. 

In the process of enamel dissolution, the bacteria may enter the 
crevices formed by solution of the interprismatic cement substance, 
and by repetition of the process gain access to the dentin (Fig. 283). 

The form of the enamel may be retained until and even after 
decalcification has reached the dentin. Clinically, this is seen as an 



276 



DENTAL CARIES 
Fig. 278 




Superncial approximal caries of enamel with films; also shows slight approxima) 

abrasion. (Miller.) 



Fig. 279 




Budding of spores on the stems of Leptothrix racemosa. (Williams.) 



PATHOLOGY AND MORBID ANATOMY 



277 



opaque white or discolored spot, resisting the instrument until some 
force is used, when it rapidly breaks down (Figs. 278 and 284). 

A central cavity, or several minute openings, leading to or almost 
to the dentin, is sometimes seen in the general decalcified area. It 
signifies the loss of the organic matter of the enamel, by unbinding or 
peptonizing actions. The extraction of an approximating tooth 
permits the film to be rubbed off, or prevents the retention of carbo- 
hydrate media, so that the bacteria cease to be active, and this spot 
may remain indefinitely at this point — e. g., the disease is arrested. 
It may cease spontaneously to develop further, owing to the estab- 

Fig. 280 




A form of streptococcus found abundantly in mouths where very rapid decay of teeth 
is in progress. X 750. (Williams.) 



lishment of an immunizing systemic change, even though the teeth 
remain in approximation, and strict prophylaxis will usually arrest 
the advance of the process. 

It is also noted clinically and microscopically that the decalcifica- 
tion is deepest at a spot just above the point of contact, and less 
deep at points buccal or lingual, occlusal or cervical, to this spot, 
and still less at points more buccal or lingual — i. e., it shades off to 
zero lingually, buccally, occlusally, and cervically (Fig. 284). The 
dentin may in such cases be deeply affected even before enamel con- 
tour is lost. Bacteria growing in the spaces from which the inter- 



278 DENTAL CARIES 

prismatic cement substance has disappeared, causes detachment of 
masses of partially decalcified rods (Fig. 285). 

When the entire thickness of the enamel is penetrated and the 
dentin attacked, there is a change in the mode of progress of the 
decalcification, which proceeds along the line of union between the 
enamel and dentin, as well as directly into the dentin (Fig. 284); in 
this way the enamel is attacked from its dentinal side (backward 
caries) (Fig. 282). 

Fig. 281 




Section of human bicuspid, showing commencement of caries: a and a 1 , appearances 
caused in enamel and dentin by the acid of decay; b and 6 2 , shreds of a felt-like mass 
of bacteria raised from the surface of the enamel; c, a cavity. X 12. (Williams.) 



In the ultimate breaking down of the enamel the rods first separate; 
the outlines of the several globules of which the rods are composed are 
brought into plain view; next, the calcified plasmic strings noted in 
enamel formation become evident; and finally, the bead-like masses 
upon these strings are left as the ultimate granular detritus of the 
enamel. 

Some of thejbacteria in the plaque are not acid producers, and it 
may be that if^a film is composed entirely of these, they may occupy 
a field and really protect it by excluding acid-forming bacteria. 



PATHOLOGY AND MORBID ANATOMY 



279 



Caries of Nasmyth's Membrane. — Miller 1 demonstrated that the 
enamel cuticle may act as a breeding ground for many forms of 



Fig. 282 




Section of carious tooth, showing appearances of decay in enamel and dentin at the 
line of union of these tissues; the dark spots shown in the enamel and dentin are 
masses of microorganisms. X 250. (Williams.) 



Fig. 283 




•^Xuii 



Penetration of bacilli between enamel prisms after solution of interprismatic cement 

substance. (Miller.) 

1 Microorganisms of the Human Mouth, 1890, and Dental Cosmos, 1900. 



280 



DENTAL CARIES 



bacteria which occupy it, forming a matrix which may retain minute 
particles of food, which in turn aid in acceleration of the progress 
of decay (Figs. 284, 288 and 290). 

Caries of Dentin. — The bacteria, after penetrating the substance 
of the enamel, attack the dentin. This presents a different anatomical 
and chemical structure to be acted upon. Beneath the enamel, the 
first layer of dentin is of a composition which permits the bacteria 
to rapidly spread laterally along this zone. They also enter the 

Fig. 284 




Decalcification of enamel without loss of form; a, film. X 35. (Miller.) 



tubules of the dentin, and penetrate by multiplication, toward the 
pulp. A wedge-shaped area of decay is produced (Figs. 284 and 291). 

In all cases decalcification precedes these invasions. At the 
periphery, the tubules communicate freely by their lateral branches 
(Fig. 289), and the lateral spreading of the bacteria by multiplication 
is readily explained. 

It is seen clinically in caries, that a portion of the dentin is abso- 
lutely destroyed and removed, leaving within the tooth a "cavity of 



PATHOLOGY AND MORBID ANATOMY 



281 



decay," bounded by dentin and enamel undergoing disintegration; 
beneath this lies dentin less affected, and beneath this, sound dentin 
(Fig. 291). These phenomena require explanation. 

The tubules of the decalcified dentin become packed for a distance, 
with bacteria (Fig. 289). These act upon the organic matrix of the 



Fig. 285 




Cover-glass preparation from scrapings of white, opaque, decaying enamel; the 
cement substance between the rods is seen to be dissolved away, and the crevices thus 
formed are filled with round and oval forms of micrococci and bacteria. Stained by 
the Gram method. X 450. (Williams.) 



decalcified tubule walls. The internal pressure due to multiplication 
distends them so that the lumen is enlarged. At the same time, the 
bacteria excrete a ferment or ferments which cause the wall at first 
to thicken. The dilatation and thickening together cause the com- 
pression of the decalcified intertubular substance, and the tubules 



2S2 



bENTAL CARIES 

Fig. 286 




Various forms of micrococci and bacteria from decaying enamel. Photographed by 
Mr. Andrew Pringle from Williams' cover-glass preparation. X 1000. (Williams.) 




Cover-glass preparations of scrapings from decay of enamel; shows Leptothrix 
buccalis maxima and Bacillus buccalis maximus, of Miller. Stained by Gram method. 
X 830. (Williams.) 



PATHOLOGY AND MORBID ANATOMY 



283 



assume a hexagonal shape owing to the mutual pressure (Fig. 293). 
The phenomenon is not a vital one, as it occurs in artificial caries. 
(Miller.) 

Fig. 288 




Enamel cuticle permeated by bacteria (1100 to 1.) (Miller.) 
Fig. 289 




Carious dentin, stained with fuchsin to show microorganisms. The section shows 
the condition of the tubules as rilled with microorganisms along the junction of the 
dentin with the enamel at a. The tubules are very much enlarged. (1/10 immersion 
objective.) (Black.) Also explains anastomosis of fibrils and indirect transmission of 
sensation. (Editor.) 



The bacterial ferment possesses a digestive or peptonizing power, 
analogous to trypsin, and begins to liquefy the inner surface of the 
tubule wall. As it does so, the lumen is further increased and the 



284 



DENTAL CARIES 



bacteria fill the acquired space. Taking up carbohydrates, lactic 
acid is produced, which combines with the calcium salts of deeper 
tubules and intertubular substance and prepares a path of decal- 
cified tissue for bacterial advance (Fig. 294). This decalcified tissue, 
to all intents and purposes, becomes a culture medium. Calcium 
lactophosphate, calcium lactate, and magnesium lactophosphate are 
produced. 

As stated by Howe some of the bacteria can withstand even 14 
per cent, of lactic acid though, of course, decalcification neutralizes 
acid which is again produced by fermentation of arriving carbohy- 
drates. Kirk has theorized that bacteria find in dentin a fermentable 

Fig. 290 




Persistence of Nasmyth's membrane in occlusal fissure. (M. T. Barrett.) 

carbohydrate food substance which leads them in that direction. 
Gies 1 states that a glyco-protein is to be found in dental substances 
and remarks that this lends color to the theory. 

The bacterial ferments continue to digest the wall of the tubule, 
and a time arrives when they have penetrated its substance. The 
intertubular substance is then removed in like manner. The same 
process occurring in adjoining tubules as well, the entire dentinal 
substance in the particular area at the cavity surface is destroyed — 
i. e., liquefied and washed away (Fig. 291, a). A cavity results. 

When the process is active at a point beneath the general cavity 



Dental Cosmos, 1917, p. 1241. 



PATHOLOGY AND MORBID ANATOMY 



285 



surface, the bacteria in several adjoining tubules destroy their walls 
and the intervening intertubular substance, forming what Miller has 



Fig. 291 




Longitudinal ground-section through the crown of an inferior molar of a negro: 
E, enamel; D, dentin; C, cement; p, pulp chamber; a, large decay, from the occlusal 
surface; b, small decay, from the mesial surface; c s, cone of septic invasion and 
discoloration; e, partially decalcified and discolored enamel around the carious cavity; 
z, dark cones; z', clearer cones; z'p, oldest cones where putrefaction of the tooth cartilage 
begins; c, outer transparent zone, or zone of Tomes; s d, secondary dentin, caused by 
irritation; s' d', secondary dentin deposited by normal physiological process, recession 
of the pulp. This figure is drawn from a ground and polished section mounted in 
Canada balsam. (Gysi.) 



286 



DENTAL CARIES 



called a "liquefaction focus" (pi. foci) (Fig. 295). This action pro- 
ceeds until the enamel is undermined and the pulp is exposed. A 

decalcified area always exists in advance 
FlG * 292 of the tubule invasion, sometimes large 

masses being found, though it lessens in 
quantity as the pulp is approached. As 
the enamel is undermined by the carious 



Fig. 293 



Carious dentin, showing in- 
invaded tubules and uninvaded 
but decalcified intertubular 
substance. (Miller.) 






«pgr 



Cross-section of decayed dentin: the tubules 
through reciprocal pressure have assumed the 
shape of five- and six-sided prisms. (Miller.) 



process, the bacteria and their acids decalcify its inner surface, the 
process proceeding from within outward, and termed "secondary 
caries," or "backward caries," of enamel (Figs. 282 and 304). 



Fig. 294 




Section of decalcified dentin partly invaded by bacteria: a, uninvaded zone. (Miller.) 



The enamel is thus weakened and at the same time deprived of 
dentinal support, and breaks down under stress of mastication. 



PATHOLOGY AND MORBID ANATOMY 



287 



Any interglobular spaces in the dentin being filled with transi- 
tional or uncalcified material like the tubule walls are rapidly invaded 
by the bacteria during their progress along the tubules (Fig. 297). 

The character of the organisms in the tubules and the nature of 
the liquefaction seem to depend upon the particular germs present. 

Miller has shown that in the deeper portions of tubules micrococci 
appear to predominate over the rod forms, which are also present; 



Fig. 295 



Fig. 296 





I 



Liquefaction foci. (Miller.) 



Decayed dentin showing a 
mixed infection with cocci and 
bacilli. X 400. (Miller.) 



although one tubule may be filled with cocci and its neighbor with 
rod forms (Fig. 296). It is only in the more superficial layers that 
the thread forms are found in numbers. 

Goadby 1 has done much interesting work in this direction, and 
offers the following classification of bacteria found in decayed dentin 
to which list must be added those found by Howe and as hinted by 
him may largely be accidental. 

1 Mycology of the Mouth, and Dental Cosmos* 



288 DENTAL CARIES 

Bacteria of Dental Caries. 
Acid-forming Bacteria. 
Streptococcus brevis 



Superficial layers of carious dentin. 



B. necrodentalis \ Deep layers of carious dentin. 

Staphylococcus albus 
Streptococcus brevis 

Sarcina lutea 

Sarcina aurantiaca ... 

Sarcina alba (Eisenberg) . . \ Su P erficial la y ers of ™™™ dentin 

Staphylococcus albus 

Staphylococcus aureus ... J 

Bacteria which Liquefy Dentin (Decalcified.) 

None isolated as yet .... Deep layers of carious dentin. 
B. mesentericus ruber 
B. mesentericus vulgatus 
B. mesentericus fuscus . 

B. fervus 

B. gingivae pyogenes 

B. liquefaciens fluorescens motilis 

B. subtilis 

Proteus Zenkeri 

B. plexiformis 

Goadby states that his experiments show that the bacteria which 
dissolve blood serum also digest decalcified dentin, while those which 
only liquefy gelatin do not digest decalcified dentin. 

His experiments also indicate that of the bacteria found in the 
superficial layers of carious dentin some produce digestive enzymes, 
others acid fermentation, and others have both functions. 

Choquet 1 has confirmed the observation of Miller, Vignal, Gallipe, 
and Goadby that the deeper the portions of dentin examined, the 
fewer species of fungi are found in the tubules, and explains it upon 
the ground that the anaerobic or facultative aerobic organisms in the 
outer layers advance into the deeper dentin, because they are better 
suited to the conditions. Kirk advances the as yet unproven idea 
that these bacteria grow toward the pulp, because that is the direc- 
tion of their food supply, i. e., the juices in the protoplasm of the part. 
In this connection, the demonstration of Goadby that some bacteria 
liquefy decalcified dentin shows that this substance is a food supply. 

These exact findings are interesting as bearing out the general 
demonstrations of Miller; at the same time, Miller's experiment 
showing absolute dissolution by a single bacterium in pure culture is 
to be recalled. (See page 247.) 

Choquet 2 has shown that dental caries may proceed under fillings 
against sound dentin by the following experiment: 

Artificial cavities were prepared in the incisors of a sheep. In these 
was securely sealed with cement, a small particle of a gelatin culture 

1 Microbes of Dental Caries, Dental Cosmos, 1900, 

2 Ibid. 



PATHOLOGY AND MORBID ANATOMY 289 

of caries fungi, applied on a sterilized platinum cap. Nine months 
later the dentin had become yellow, slightly decalcified, and the 
tubules penetrated by bacteria. This softened dentin was used to 
inoculate a portion of the medium originally used, and the species 
again cultivated. 

Miller 1 estimated the relative loss of inorganic and organic matter 
in dentin during the process of caries, by weighing and analyzing 
equal volumes of carious and sound dentin from the same teeth. 





Fig. 297 


'■■■■■< // / 


fJsM./ / -//. i 






i j 


4f - 


• 




ijj! 1 ' 1 '' 


^ ; ^/?l 


Interglobular spaces 


filled with bacteria. (Miller.) 



The carious dentin had lost about seven-ninths of its weight, 
which was due to the loss of twelve-thirteenths of its original calcium 
salts by decalcification, and two-fifths of its original organic matter 
by liquefaction of its substance. 

Tube Casts. — In the zone of decalcification, in advance of bacterial 
invasion of the tubes, are found rod-shaped bodies or shining granules, 
first described by J. Tomes. They occur in both 
natural and artificial caries, hence it must be FlG - 298 

inferred that their presence is not the result of a 
vital process. 

The rods do not dissolve in organic acids, 
but dilute sulphuric acid quickly dissolves 
them. They are unaffected by alcohol or 
chloroform, a proof that they are not composed 
of fat. Miller regards them as probably calcic 
formations against the tubule wall as a cast of 
the wall, and which become loosened when en- Tube casts. 

largement of the tubule occurs. They have a 
tubular structure, are brittle, and may contain a central thread-like 
filament which may possibly be the remains of a dentinal fibril. 

1 Microorganisms of the Human Mouth. 
19 



290 



DENTAL CARIES 



Bacteria may surround them, but do not enter them. The granules 
are probably broken rods. 1 The data point toward a probability 
that the rods are composed of calcium lactate and calcium lacto- 
phosphate, the result of a combination of lactic acid with the calcium 
salts of the dentin. The resultant salt is probably deposited as a 
tube cast, as suggested by Miller. 

The Transparent Zone. — Around the zone of decalcified uninfected 
dentin appears a zone of dentin more transparent than the surround- 
ing normal dentin. The zone extends from periphery to periphery 

Fig. 299 




Section from a lower incisor worn on a plate, extensive decay without increase of 
transparency. X 15. (Miller.) 

around the cone of carious dentin (Fig. 291, c). The tubules in this 
area contain granular matter not seen in normal dentin, nor in the 
dentin of dead teeth in the same situation. 2 

Tomes and Magitot both regarded the transparency as an attempt 
made by nature to impede the progress of caries. Walkhoff regards 
it as due to a sclerotic action, the fibrillse upon stimulation producing 
intercellular substance (tubule wall), at their own expense and 
primarily of their offshoots. Miller advanced the following data. 3 



1 Microorganisms of the Human Mouth, 



2 Ibid. 



3 Ibid. 



PATHOLOGY AND MORBID ANATOMY 



291 



1. Transparency indicates increased homogeneity as opposed to 
the heterogeneity of normal dentin — i. e., the coefficients of light 
refraction are brought nearer together. 

2. It occurs in living dentin only and is not found in natural teeth 
mounted on plates and decayed in the mouth, nor in secondary caries 
of dentin from the pulp cavity to the periphery, and is, therefore, a 
result of vital action. (Compare Figs. 291 and 301 with Figs. 299 
and 300.) 

3. The tubules have their lumen lessened in diameter in the trans- 
parent areas, an agreement with the position of Walkhoff. 

Fig. 300 




Secondary caries of dentin, advancing from pulp chamber and therefore occurring 
after death of the pulp. Absence of transparency. X 15. (Miller.) 



4. Secondary dentin may accompany the process in contiguity 
with the area; moreover, secondary dentin is translucent. It indi- 
cates a constructive excitation of the odontoblasts, of which the 
dentinal fibrils are prolongations (Figs. 291, Sd). 

5. Chemical analysis proved that no lime salts had been lost, and 
it was pointed out that a gain in the percentage of salts was unneces- 
sary, as new dentin is necessarily composed of organic as well as 
inorganic matter, wherefore the analysis would not necessarily vary 
from that of normal dentin. 



292 



DENTAL CARIES 



6. It is found in connection with abrasion of human teeth in which 
the activity of acid may possibly be an open question, and it also 
occurs in the worn teeth of dogs, the saliva of which is strongly 
alkaline. 

Miller states that opacity may follow or be associated with trans- 
parency. 1 

The natural conclusion is that the transparency is a form of 
tubular calcification, and that it impedes the progress of caries; that 
it does not succeed, as a rule, is due to the overwhelming action of 
the bacteria. 

Fig. 301 




Transparency resulting from cracks in the enamel at a and b. X 20. (Miller.) 



In cavities from which the walls are broken away, freely exposing 
the carious dentin to mastication, the carious dentin and its con- 
tained bacteria may be removed by friction (Fig. 305, B). 

Transparency may begin even before caries has penetrated the 
enamel 2 and Fig. 301 shows that it may begin before the enamel is 
worn away. There would seem to be some possible fibrillar relation 
in such cases (see page 144). 

In the transparent area, the tubules become obliterated ; a polished, 
discolored surface results, resembling in degree an abraded surface. 

1 Dental Cosmos, April, 1903. 

2 Kirk, in Fones' Mouth Hygiene, p. 200. 



PATHOLOGY AND MORBID ANATOMY 293 

This process is called "eburnation," and is really tubular calcifica- 
tion (which see). In the same tooth a more sheltered border of this 
spot may be undergoing the carious process. Miller records cases of 
badly decayed teeth, in which the process ceased spontaneously and 
the dentin became hard and smooth. 

Pigmentation in Caries. — Pigmentation occurs in caries possibly 
from extraneous substances entering the carious area, possibly from 
the substances formed during putrefaction. 

The slower the progress of the decay, the greater the discoloration. 
The colors vary from light yellow to reddish brown, dark brown, 
and black. 

The color is, as a rule, darkest upon the outside of the carious 
dentin, but the pigment may extend through large masses and be 
found staining dentin beneath the caries, hard enough to leave in 
situ. As a rule, this is not the case. 

Black suggests the possible formation of sulphids. Miller has 
found iron almost constantly present in carious dentin. The dis- 
coloration of dentin does not seem to be necessarily due to the 
carious process, as it may be seen in areas of abrasion. In a specimen 
possessed by the editor, a limited cervical caries caused a growth of 
secondary dentin and an area of tubular calcification. From the 
pulpal surface of the secondary dentin to the area of caries, extends 
a sharply defined area which has a flesh-rose color (Fig. 302). Many 
areas of secondary dentin due to abrasion are stained a dark 
brown. 

Artificial caries produced in teeth placed in a mixture of bread 
and saliva, and the mixture constantly renewed, was white. If putre- 
faction was allowed to occur, discolorations ensued (Miller). 

The discolorations of carious dentin may be due to the action of 
chromogenic bacteria. Miller isolated from the mouth, an organism 
which he named Bacillus fuscans, and "which, cultivated on the 
surface of nutritive agar-agar, in a few weeks imparts to the medium 
a yellowish-brown color, which gradually darkens and extends 
deeper into the substratum as the age of the culture increases." 

It is significant that the three acid-forming organisms found by 
Goadby, in the deep layers of carious dentin, do not form pigment 
in their artificial media. The action of acidific bacteria may yet be 
shown to be responsible (see page 250) . 

Caries of Cementum. — Caries of cementum occurs when the gum 
has receded, exposing the cementum to the fluids of the mouth. As 
a rule, a triangular depression exists bounded by the thickened gum 
margin, the cementum, and the enamel. This favors the collection 
of the bacterial plaques, and caries follows. The gum may be much 



294 DENTAL CARIES 

receded, yet no caries occurs. As a rule, however, recession and 
uncleanliness frequently assure its presence. Especially is this true 
in cases of general recession in aged or debilitated persons. (Fig. 302) . 
The path of bacterial invasion after decalcification, is by way of 
Sharpey's fibers to the lacunar and canaliculi; later the dentin is 
invaded as in the crown. Frequently the form of the cementum is 
largely retained, while the decalcification is deep. 

Fig. 302 ' Fig. 303 




Cervical caries associated with secondary Caries of cementum and dentin com- 

dentin. Area pigmented. pletely encircling the tooth. 



CLINICAL HISTORY OF CARIES. 

The clinical history of dental caries records the observable phe- 
nomena associated with its inception, progress, and termination. 

Inception of Caries. — Caries begins, after the manner described 
in the pathology, at favoring spots. As a rule, in molars the occlusal 
fissures are first decayed, being often carious in this situation before 
fully erupted. Uninformed parents usually consider the first perma- 
nent molar a temporary one, and frequently neglect it. It moreover 
has often seriously defective fissures, which afford lodgement for 
microbic plaques, which seem to be readily formed because of the 
unhygienic state of the temporary teeth, which are frequently 
carious, and the permanent molars are unbrushed during eruption. 
Not infrequently a cavity is produced on the mesial surface of this 
tooth by a carious condition of the distal surface of the second 
temporary molar. In other mouths, both teeth are affected alike, 
owing to the nature of the approximation. The relative liability of 
the various surfaces of the different teeth to caries may be averaged 
for a great number of persons, but tables drawn from clinical cases 
may have little application to a particular individual, as peculiarities 
of local predisposing causes and personal habits modify the inception. 
Nevertheless, such tables are exceedingly interesting as showing a 
general relative liability. 



CLINICAL HISTORY 295 

The following is from the U. S. Army report, 70,000 teeth being 
filled. 

Average percentage 
Teeth. of each carious. 

First permanent molars 6.5 

Second permanent molars 5.1 

Upper central incisors 3.9 

Premolars 2.8 

Third molars 2.0 

Upper canines 1.7 

Lower incisors 0.7 

Lower canines 0.5 

The lower anterior teeth are the last of all to be affected, and it is 
common to see the six lower anterior teeth free from caries, years 
after all of the other teeth have been lost. This is attributable to 
the constant motion of the saliva, the presence of calculus, and to 
the mechanical effects of tongue movement, lip movement, and 
mastication. 

In the temporary set, the molars decay much more frequently than 
the incisor teeth, partly because longer retained and partly because 
of the width of their approximations. The pulp is readily exposed 
because of its relatively larger size. 

Approximal cavities are frequently more broad than deep, and 
present problems of anchorage. 

The Progress of Caries. — The rapidity of progress of caries depends 
upon the intensity of the action of the exciting cause, the structure 
of the tooth, and the nature of the vital resistance offered. The 
exciting cause will act most intensely in mouths ill-cared for, and 
containing much carbohydrate debris, and these conditions being 
equal, enamel of poorer organization and presenting a greater degree 
of solubility, in teeth presenting broad approximations, will be the 
more rapidly destroyed. Caries does not begin, but may spread 
under the gum. 

Williams has expressed the opinion that, as a rule, the process of 
enamel destruction occupies a considerable period of time, a fact 
which may account for the general lack of caries in the temporary 
teeth until about four or five years of age. 

The decalcified enamel may retain its form for a time after dentin 
decalcification has begun. An opaque spot, often discolored, is 
seen upon the tooth, and is readily broken down by an instrument 
before dentin decalcification occurs, though such decalcification is 
often found. If the approximating tooth be extracted, the carious 
process may cease, owing to the removal of the bacterial plaque, or a 
lack of food supply (retention). This result may not follow, if the 
dentin has been invaded before the extraction. 



290 



DENTAL CARIES 



After enamel destruction at a limited area, caries progresses along 
its inner side and penetrates the dentin. The enamel is undermined. 
The extent of cavity orifice is no certain guide as to the depth of 
penetration. The under surface of the enamel then decalcifies. This 



Fig. 304 











Caries undermining enamel: a, masses of bacteria lining the cavity. X 50. (Miller.) 
This may lead to the appearance in Fig. 306. 




is backward or secondary decay of enamel, and causes an opaque 
appearance of the undermined enamel. (Figs. 304, 305, A.) 

Cases are frequently observed, in which the only external evidence 
of caries, in a molar or bicuspid, is a white or bluish-black line marking 



CLINICAL HISTORY 



297 



the fissure, and yet the dentin may be deeply and widely penetrated 
(Fig. 305, A). 

As a rule, however, as the cavity in the dentin enlarges, the enamel 
at the orifice becomes disintegrated, so that the orifice is enlarged 
and more food debris enters to accelerate the process (Fig. 291). A 
deep and wide cavity may thus be formed before the patient is 
objectively or even subjectively aware of its existence. After a 
time, the occlusal enamel boundary of the cavity breaks down and 
food is even more readily admitted. 

It has been noted that if the enamel break away in such a manner 
as to expose the carious dentin to the friction of food masses which 
are not retained and to the access of saliva, the progress of the 
caries is delayed and in some cases ceases altogether. The process 
of eburnation is set up. (See Transparent Zone and Tubular 
Calcification.) (Fig. 305, B.) 

Fig. 306 




Spreading caries in a molar with some enamel remaining. Fig. 304 will 
explain the process. 



The process is sometimes seen in certain cases in which caries 
has followed the dento-enamel junction, the enamel chipping off 
as undermined, so that almost the entire superficial portion of the 
dentin may be subjected to this process and remain of original form 
and discolored and eburnated. This is "spreading caries" (Fig. 306). 
In other cases the tubules are followed and the pulp is rapidly 
approached. This is "penetrating caries' ' (Fig. 291). 

Caries may progress rapidly for a period, and then receive a check 
to its progress. Teeth previously free from the disease may suddenly 
fall victims to its rapid and widespread progress. No doubt, in many 
of these cases, there are removed from or added to the local oral 
conditions, constitutional influences which deter or favor the local 
development of caries producing bacteria. The editor has the models 
of the jaws of a boy, aged fourteen years, with every tooth but three 
decayed to the gum, and the three teeth contained six cavities. 

Secondary dentin is less readily decalcified than primary dentin. 



29S DENTAL CARIES 

The dentin of pulpless teeth is more rapidly invaded after enamel 
decalcification than that of vital teeth, owing to the absence of vital 
resistance. This condition does not necessarily apply to the enamel 
of pulpless teeth. 

While caries appears at all ages from childhood to old age, its 
ravages are most pronounced and its progress most rapid during the 
period of adolescence and early maturity. Its effects are most 
marked between the ages of eight and twenty-five years. As a rule, 
a denture which remains at tw r enty-five years unaffected by caries, 
remains unaffected or but slightly affected to an indefinite age. To 
be sure, this implies two conditions: (1) That the active causes of 
caries have been in but slight evidence, and (2) that the denture is 
of the highest order. The classes of dentures which escape are per- 
fectly formed and symmetrically arranged teeth, in the mouths of 
patients who lead sanitary lives and care for the teeth, who masticate 
vigorously, and who escape other diseases. Very filthy dentures 
may escape, owing, as stated, to putrefaction (See page 271.) 

Caries beginning at the junction of the cementum and enamel of 
the teeth has a somewhat different clinical history from that noted 
when its occurrence is in other situations. Its progress is subject to 
great variations. In any of the catarrhal conditions or atrophic 
conditions of the gum which lay bare the neck cementum, caries 
usually occurs. This is usually situated at the middle of the cervix 
in the cementum, though in cases of recurrence of caries, it is often 
at the labial or lingual proximal cervix. It occurs also as a process 
secondary to labial abrasion and erosion of the teeth especially at the 
cervical curve. Teeth affected by erosion, however, are commonly 
exempt from dental caries. 

The Terminations of Caries. — After the pulp is exposed, it sooner 
or later becomes inflamed and hypertrophies or dies. In the latter 
case putrefaction results, which for a time may exert a restraining 
influence upon decay, but not for a long time. 

Masses of food freely enter the pulp cavity and caries proceeds in 
the dentin from within toward the periphery. This is " secondary or 
backward caries" of dentin, and as it occurs in dentin without vital- 
ity, no transparency results (Fig. 300). Notwithstanding, caries at 
this stage proceeds rather slowly, particularly if the crown be much 
broken down. The result of secondary caries is a hollowing out of 
dentin of the root, and finally a decalcification of the cementum, 
which may persist for some time as a thin, elastic wall. Finally this 
is destroyed either at the occlusal periphery, or caries causes pene- 
tration to the pericemental tissue. This may occur laterally or 
through to the bifurcation of the roots. In either case it is called 



SYSTEMIC EFFECTS FROM CARIES 



299 



"perforation by caries." Into this perforation the pericemental 
tissue may become protruded by hypertrophy, and the condition 
of hyperplastic or fungous gum be established. Following the 
breaking down of the crown, the blood pressure in the pericementum 
begins an extrusive process, the pericementum becomes thickened, 
and the tooth is somewhat loosened. 

Decay of the root face and interior, and breakage of the ceniental 
margins proceed eventually with the extrusion, until finally but 
a small discolored bit of the root end lies upon the surface of the 
gum, from which it is removed by some slight force or is extracted. 

The entire process of caries in a tooth may thus extend over a 
period of from ten to twenty years. 



Fig. 307 




This root has been unsuspected in this position for over twenty yean 
spot on the gum overlying it being the only indication. 



a small blue 



At times the extrusive force pushes a root up sidewise, particularly 
when the tooth has been tipped over before the loss of the crown. 
It may thus be retained in position and attached upon its under side 
for some time. The upper side may be polished by abrasion. The 
exposed end of a root undergoing extrusion is also sometimes made 
smooth by abrasion. A bit of root left in situ after breakage during 
extraction usually undergoes the same process of extrusion, but may 
not decay until it comes under oral influences. Usually a sinus leads 
to such a root, but the gum may heal over it (Fig. 307). 

Such a root may at any time become the source of apical abscess 
or of an intractable neuralgia, the cause being only determinable 
by radiography. 



SYSTEMIC EFFECTS FROM CARIES. 

The presence of cavities, calculus, and pyorrhea alveolaris in the 
mouth all tend to cause infection of the digestive tract, with produc- 
tion of inflammatory (catarrhal) disturbance, and to cause infection 
of parts in close association with the teeth as well. 



300 DENTAL CARIES 

Undoubted cases of septic intoxication and infection from decayed 
teeth and other oral conditions have been reported, the connection 
having been shown by their cure after removal of the local cause 
alone; in other cases the parts (as the stomach) having the secondary 
infection well implanted, have required special treatment in addi- 
tion to the removal of the primary exciting cause. 1 (See Systemic 
Effects of Pyorrhea Alveolaris.) 

The loss of masticatory efficiency due to caries or the associate 
pain has a direct bearing upon insalivation of food and upon gastric 
digestion, though in this connection bacterial infection may play a part. 

Insomnia and a variety of other metabolic ills have been shown to 
be due to carious teeth and the sepsis associated, by the prompt or 
gradual recovery upon removal of the teeth. How many thousands 
of individuals suffer from partial sepsis, in entire ignorance and 
possibly without actual discomfort can only be conjectured. It is 
exceedingly difficult to state positively that a metabolic disorder is 
due to the state of the mouth, unless a microscopic examination from 
a separate locality demonstrates identical bacteria present. Even 
then the therapeutic test must decide. Therefore general deductions 
must govern advice. In all cases it is wise to put the mouth into a 
hygienic state and, if necessary, add such other therapy as the 
systemic condition demands. 

School children who suffer much from caries are apt to be less 
proficient in their studies than normal children, the effect being 
probably due to that of disturbed digestion upon metabolism and 
thus upon mentality in general. Pain, of course, is a direct cause 
reducing vitality in various ways and causing loss of time and atten- 
tion to the duty of study, etc. The following quotation from a 
tabulation 2 shows typically the effect of dental normality upon 
mental powers. It has the lowest gain, which ranged from about 
32 to about 918 per cent. 

Per cent, of 
Beginning. Present. Diffeience. gain or loss. 

Memory 66.65 66.6 00.05 00.07 

Spontaneous association . . . . 74.25 90.7 16.50 22.22 

Addition 46.00 63.0 17.00 36.95 

Association by opposite . . . . 59 . 00 92 . 33 . 00 55 . 93 
Quickness and accuracy of perception 41.50 60.5 19.00 45.78 
Total gain .... 32.162 per cent, after deducting the losses. 

1 Hunter: International Dental Journal, 1899, abstract from Transactions of 
Odontological Society of Great Britain. 

In an address at McGill University, Montreal, in 1910 (see Dental Brief, November, 
1911). Hunter reaffirms extensive experience with gastritis, septic anemia, septic 
endocarditis, etc., as the result of oral sepsis in which decayed roots and extensive 
dental work, (bridge, etc.), covering septic conditions were the causes and which were 
cured by removal of the cause. While caries was not separately considered, it must 
be seen that caries is largely responsible, for the inception of the conditions though 
pyorrhea is also responsible. 

2 Dental Brief, 1911. Tabulation of the Effects of Dental Caries on the Mental 
Powers of the Dental Class in Marion School, Cleveland, Ohio. 



CHAPTER X. 

DENTAL CARIES: DIAGNOSIS, SYMPTOMS, AND 
PROGNOSIS. 

DIAGNOSIS OF DENTAL CARIES. 

The diagnosis of dental caries is made through both objective and 
subjective symptoms. The signs are the existence of cavities and 
of softened areas, directly visible or made evident through instru- 
mental means. The symptoms are pains of several degrees of inten- 
sity. The nature and intensity of the pains furnish a guide to the 
depth of the carious invasion, and but an indirect indication of the 
location of the disease. 

Diagnosis by Objective Symptoms. — The presence of the markings 
of superficial decay, decalcified surfaces, or cavities may often be 
detected at a glance or be seen reflected in a mouth mirror. Opacity 
of enamel is usually due to its superficial decalcification or caries 
beneath it, though at times a malformation may exist. Sometimes 
a zinc phosphate lining will cause an opacity resembling backward 
caries of enamel. The discoloration or opacity about a fissure or 
occlusoproximal or bucco- or linguoproximal surface should excite 
suspicion of caries. In the routine examination for cavities, sharp, 
finely pointed explorers bent at various angles are to be passed over 
all the surfaces of the teeth. If the enamel at any point admit the 
point of the explorer, caries is usually present. Fissures are some- 
times deceptive in this respect. A good rule is to adjudge the pres- 
ence of caries when the point catches slightly as removed. It is well 
to remember in this connection, that an unsuspected adjunct fissure 
will often contain beneath it caries deeper than the central point 
judged defective. All fillings which admit of penetration between 
the filling and margin are defective often permitting much caries 
under the filling. This is especially true in case of unextended 
occlusal fissures (see also Recurrence of Caries). 

In the search for approximal caries great care is required, explorers 
with very short points being often necessary, as long points will not 
turn into the cavity owing to the close contact. The ordinary No. 7 
explorer has not a short enough tine. Frequently a cavity may 
only be discoverable from one point of access, so that the approximal 

(301) 



3or 



DENTAL CARIES 



Fig. 308 



Fig. 309 




Explorer 
for caries. 
(Jack. 1 ) 






Dow electric lamp for mouth illumination, with 
reflectors. Reflector A is jointed to vary the angle of 
reflection. Reflector B is for illumination of the 
fauces. Reflector C is for lateral illumination. 
(Jack. 2 ) Switchboards usually have electric lamp 
attachments. 

surfaces should be examined from the labial 
and lingual sides and also from the occluso- 
proximal aspect. In the absence of evident 
cavities, some force should be applied to 
detect softened spots of enamel. The 
catching of the explorer upon both teeth, 
after it has passed through the interspace, 
often simulates the catch in a cavity; 

Umvaxed floss silk passed over carious 
surfaces indicates a rough surface by fray- 
ing. It may, however, at times pass readily 
over a cavity easily detected by instru- 
ments; so that it is not absolutely reliable 
as a test. It also catches on a rough filling 
or protruding filling margin. If the short, 
sharp pain of hypersensitive dentin is pro- 
duced as floss passes between the contact 
points of the teeth, either a masked small 
cavity or a loose filling should be suspected, 
and if not found with the explorer or light, 
a wedge should be introduced. 

The strong light of an electric mouth 
lamp transmitted through the teeth exhibits 
a cavity as an opaque spot outlined upon 
a pinkish background. It not only permits 
an easy diagnosis, but also affords evidence 
of the depth of penetration. It often fails 
as a test in posterior teeth. Mechanical- 
separators or wedges are at times necessary 



American Text-book of Operative Dentistry. 



Ibid. 



DIAGNOSIS OF DENTAL CARIES 303 

to press apart contiguous teeth sufficiently to admit exploring 
instruments. 

The necks of the teeth should be examined with sharp points, to 
note any softness of the tooth tissues. The margins, particularly 
the cervical and neighboring margins, of every filling should be 
explored to test the integrity of the junction of filling and tooth, 
or any excess or deficiency of filling material. Where doubt exists at 
the cervix of a filling it should be remembered that caries will exhibit 
a cervical or cavity margin and a filling margin, while filling excess 
will have but one. The cervix beneath gold crowns and the joints 
of dowelled bandless crowns frequently show caries. 

The examination should be conducted by one of two systematic 
methods. In one method the occlusal faces of all the teeth are first 
examined in one survey, then the proximal surfaces, and lastly, 
the buccal and lingual surfaces of the teeth. In the other method, 
every portion of each tooth is examined, beginning with a central 
incisor or terminal molar, before passing to the adjoining tooth. Any 
cavity or condition found should be noted upon a diagram for refer- 
ence at sittings. This is preferably done at once so it will not be 
forgotten. 

Diagnosis by Subjective Symptoms. — Complaints by patients 
that cold or hot, salt, sweet, or acid substances taken into the mouth 
cause unlocalized or partly localized pain, indicate exposed and 
hypersensitive dentin or pulp exposure. Such complaint is to have 
due consideration. Slight pain has also been produced by the 
passage of floss over a minute cavity unexplorable before wedging, 
and is probably due to compression of liquid upon dentine. This 
symptom at the cervix of a tooth indicates hypersensitive exposed 
dentin which may or may not be carious. 

Pain beginning without the application of special stimuli, is like- 
wise ordinarily connected with caries or its sequelae, and should be 
taken into account. 

Pain produced upon mastication has either the significance of 
pressure on fibrils or pulp, or is a symptom of pericemental irritation. 
Such irritation complained of by patients after even careful attention 
is not uncommon and should lead to rigid search for masked cavities, 
hypersensitive occlusals or caries, marginal gum irritation" or septic 
or non-septic pericementitis. Much harm is done by inefficient 
diagnosis of cavities which may later enlarge and expose the pulp. 
In view of the doubtful success of root canal treatment this is very 
important. 



304 DENTAL CARIES 

PROGNOSIS OF CARIES. 

If existing caries be promptly treated in youth and a proper sys- 
tematic prophylaxis be employed, its recurrence during youth may 
be largely prevented. At about adult age a fair degree of immunity 
may be expected. In the absence of treatment or prophylaxis, the 
exciting causes seem to become very active, and many teeth may be 
lost from caries or by reason of extraction for- pulp and pericemental 
diseases. Extraction itself brings many evils in its train. (See Non- 
septic Pericementitis.) 

Even advanced caries may be checked by proper filling or crown- 
ing, and if then prophylaxis receive due attention, the prognosis 
for the teeth is generally good; indeed, it seems as though but few 
conditions exist dependent upon caries alone except in advanced 
caries of roots which are not subject to correction by some of the 
means within the resources of the profession. 

HYPERSENSITIVITY OF DENTIN. 

Normal dentin has a varying degree of sensitivity as shown when 
sound crowns are ground or sound dentin drilled, therefore only 
hypersensitivity induced by some abnormal circumstance can be 
considered a pathological entity. 

Therefore it may be defined as such a degree of fibrillar sensi- 
tivity as interferes with comfortable instrumental work upon dentin 
or which in the absence of dental ministrations causes painful symp- 
toms as a rule reflected about neighboring parts. 

Anatomical Data. — The dentinal tubules contain the prolongations 
of the odontoblasts left behind in their progression toward the physio- 
logical pulp cavity (dentin being developed from without inward). 
These so-called dentinal fibrils extend from odontoblast to the dento- 
enamel junction and into the decussated tubules at that point. 
Mummery of late has seemed to show that very fine neurofibrils pass 
"from the medullated nerve trunks of the pulp into the dentinal 
tubes," " at the periphery of the pulp and the cornua. The medullated 
fibers lose their medullary sheath and neurilemma and the axis 
cylinder spreads out into a fan-shaped expansion of neurofibrils 
which enter into an intricate plexus beneath the odontoblast layer." 
From this plexus neurofibrils pass to form a network around and 
between the odontoblasts without forming any direct communication 
with them while other larger strands of the neurofibrils pass between 
them in a more or less wavy course to the dentin margin and enter 
the dental tubules. 



HYPERSENSITIVITY OF DENTIN 305 

Fig. 310 demonstrates this. It is only fair to state that Hopewell- 
Smith 1 has denied these to be nerves and that Hanazawa 2 does not 
make any claim for neurofibrils in the tubules as the result of his 
researches. This does not mean that Mummery's technic is not 
correct but leaves the demonstration as yet disputed. 

Hitherto there have been two main contentions: 

1. That the nerves ended between the odontoblasts (Retzius). 

2. That the odontoblast possesses a long fiber extending back into 
the axis cylinder of the nerve (Robertson). 

Fig. 310 



From the cornu ot the pulp of a fully furmed human premolar, a, medullated nerve 
bundle dividing (inclosing the transverse section of bloodvessel) ; d, dentin. Neuro- 
fibrils entering the tubules. (Mummery, Dental Cosmos.) 

In case 1 the only plausible theory of pain production is that under 
irritation, a contraction of the whole cell fibril and odontoblast 
occurs (as in muscle cells), 3 the sensory endings being pressed because 
of the lateral bulging of odontoblasts (i. e. squeezed). 

In case 2 the fibrillar connection with the axis cylinder would be 
pulled, but how far the true nerve also may extend into the odonto- 
blast and dentinal fibril is left open to doubt. 

Any of the above histologies would account for pain produced by 
all classes of irritants by direct irritation or indirect irritation due to 
contraction of the whole cell. 

The theory of Gysi that a wave-like motion is set up due to incom- 
pressibility of the water or the theory that pain is due to compression 
does not seem to fit chemical or thermal irritants. 

. i Dental Cosmos, 1916, p. 421. 

2 Ibid., February and March, 1917. 

3 Black: American System of Dentistry. 
20 



306 



DENTAL CARIES 



Normally the dentin is protected from external agencies by the 
enamel, and in the early stages of gum recession by the cementum, 
though it has been shown by Choquet that the enamel may be over- 
lapped by the cementum which is usual or may overlap it or they may 
lie edge to edge or the dentin may be uncovered at this point. 

Thermal stimuli at times give evidence of their direct effect by 
producing immediate painful sensations. The pulp is stimulated 
through the nerves or the odontoblasts and their relations with the 
terminals of sensory nerves in the pulp, and a degree of vascular 

Fig. 311 




Diagram of enamel-rod directions and tubule curves. From a photograph of a bucco- 
lingual section of a superior bicuspid. (Noyes.) 



overfulness occurs which may be denominated mild hyperemia. The 
effect of these reactions is to cause the sensory functions of the pulp 
and fibrils to become somewhat exalted, and it therefore becomes 
more responsive to the stimuli. (See Arterial Hvperemia of the 
Pulp.) 

Apart from the effect of thermal changes, other substances act as 
irritants. The lactic acid and other bacterial products in the cavity 
of decay, without doubt play a part in exalting the irritability of the 
fibrils. A slightly loosened filling holds the acid in contact, as such 



HYPERSENSITIVITY OF DENTIN 307 

cases are often very sensitive. Salt, sweet, or acid substances intro- 
duced into the mouth are also evidently irritant, as active symptoms 
follow their application to hypersensitive dentin. The same is true 
of acid salts as zinc chlorid. 

Mechanical abrasion or erosion may irritate the fibrils, or at least 
expose them to the action of other irritants. As a rule, however, the 
abraded or eroded surfaces are protected from hypersensitivity by 
the process of eburnation. (See Transparent Zone.) 

The scraping of necks of teeth with scalers sometimes induces 
exposure of dentin. Within cavities of decay, the hypersensitivity 
is greatest, as a rule, at the dentinal periphery. That at this point 
the branched endings of the tubules present a greater number of 
fibrils to the action of the irritant is quite evident (Fig. 311), which 
would also be the point of greatest sensitivity in case neurofibrils are 
present. 

In cervical hypersensitivity, the cementum or enamel is removed 
by gum recession, abrasion, erosion, or caries, and the fibrils are 
exposed. The presence of the granular layer of Tomes in this situation 
and the possibility of this layer containing the expansions of the fibrils, 
are to be considered. (Fig 313, Gt.) 

In certain cases, the irritation excited by the touch of an instrument 
to dentin adjacent to enamel is carried to the pulp by anastomosing 
dentinal fibrils. This was proved by a few cases, of which the follow- 
ing is an extreme one : 

In a central incisor, secondary dentin had filled a portion of the 
pulp cavity (Fig. 312, S D). Caries had subsequently removed the 
incisal portion of this secondary growth and 
also the dentin containing fibrils leading FlG - 312 

from the pulp cavity to the middle of the 
incisal edge. The application of an ex- 
cavator to dentin in the incisal portion of 
the cavity (at A), the fibrils of which could 
have no direct relation with the pulp, pro- 
duced flashes of pain. This was unmistak- 
ably of the character of hypersensitive 
dentin. 

A professional friend claimed to feel sen- 
sitivity in a cervicolingual cavity of a molar, J^t"/^ 
in which the filaments had been destroyed sensitive dentin: s D, sec- 
by suppuration for one-third of the length SjSSS^' »*££ 
of the canals. If his contention was true, grammatic.) 
the sensation must have been conducted 

by way of the granular layer of Tomes to the level of the pulp, 
and thence by the fibrils to its substance (Fig. 313). 




308 



DENTAL CARIES 



Spots of cervical hypersensitivity have been occasionally recorded 
as occurring in teeth, the canals of which have been filled. 

Head 1 records a case in which the dentin bounding the pulp canal 
remained hypersensitive for a year after the pulp was removed. In 
this connection the possibility of the presence of a vital pulp filament 
in the pulp canal, or of irritable apical tissue receiving the impact of 
liquid forced down upon it by a canal probe, or of a pericementum 

Fig. 313 




Two fields of cementum, showing penetrating fibers: Gt., granular layer of Tomes; 
C, cementum not showing fibers; F., penetrating fibers. X 54 (about). (Noyes.) 

irritable to touch of any sort, must all have due differentiation. I 
have never seen a case of hypersensitivity of dentin in which some 
filament of pulp was not present, in at least a part of the tooth. 

Dentin cannot become inflamed in the ordinary sense, as leukocytes 
cannot enter the tubules; nevertheless, the irritability of the fibrils, 
like that of other protoplasm, may be exalted (or lessened). 

1 Dental Cosmos, 1899. 



HYPERSENSITIVITY OF DENTIN 309 

With hypersensitivity other functions are increased, and in con- 
ditions producing a constant stimulation, a constructive change may 
occur and the fibrils form tubular substances at their own expense. 
(See Transparent Zone and Tubular Calcification.) 

That the hypersensitivity is primarily, as a rule, a disease of the 
tubular contents involved, is shown by the fact that occasionally of 
two cavities in the same tooth, one will present a hypersensitivity 
and another none; again, one part of a cavity may be hypersensi- 
tive and the rest not so. 

Symptoms. — A certain degree of uneasiness of undefined character 
may at times be noted in teeth containing cavities, but, as a rule, 
pain other than pulp pain is only felt upon the application of special 
stimuli. Of course, the presence of ferments, acids, etc., in a cavity 
are real stimuli. 

The infiltration of acid, salt, or sweet substances into contact with 
a hypersensitive surface is followed by a wave of gnawing pain, 
reflected usually along the course of contiguous nerve filaments. 
While not definitely localized, owing to the fact that the pulp does 
not possess a tactile or localizing sense, the pain may usually be 
referred to a certain part of the mouth. The pressure of an instru- 
ment upon the dentin is attended by a flash of sharp pain, which 
continues for a time, but lessens if the contact be maintained. In 
this test the pain is localized in the affected tooth, the touch of the 
instrument being followed by a recognition of position by the tactile 
organ of the tooth, the pericementum. 

Occasionally, food forced by mastication against a hypersensitive 
surface, such as due to abrasion or caries in a crevice or cavity, will 
produce a sharp pain subsiding promptly, and which may not be 
repeated for some time. The mere rubbing together of opposing 
abraded surfaces may cause the symptom, and is more pronounced if 
a hard substance, as grit, gets between them. 

Cavities dried for filling usually produce a steady pain, caused by 
dryness and relieved by an analgesic or by filling. 

It is beyond doubt that individuals differ as to the degrees of 
normal dentinal sensitivity; the dentin of one person may be cut 
freely without evidence of marked pain; in another, the touch of an 
instrument to the newly exposed dentin is productive of unbearable 
pain. The difference in degree of irritability is manifested in another 
manner: If a mild sedative — for example, oil of cloves or an obtun- 
dent — be applied to the hypersensitive dentin of one person, it may 
remove the distressing symptoms, but with others it may be necessary 
to employ the most extreme measures to reduce in any degree the 
hypersensitivity. In some cases, the exposure of dentin about the 



310 



DENTAL CARIES 



necks of teeth may induce such an unbearable local pain or neuralgic 
condition as to positively demand relief. 

In a few cases enamel has exhibited sensitivity. In one case the 
effort to open sound fissures about a cavity for prevention excited 
sharp pain, ceasing upon removal of the instrument. The patient 
was, however, a sufferer from insomnia, and from the effects of 
morphine taken for it, and her dentin was exquisitely sensitive. This 
patient seen again after a lapse of many years had scarcely any sen- 
sitivity. The same phenomenon of enamel sensitivity is to be noted 
in one of her children. 



Fig. 314 



Fig. 315 




The Teter nitrous oxide and 
oxygen apparatus on apparatus 
stand. 




Gregg nasal inhaler. 



In another patient, the side of the enamel exposed by a cavity in a 
molar analogous to that in Fig. 312 gave flashes of pain when touched 
with an excavator point, though no evident direct path of trans- 
mission to the pulp could be seen. Caush's tubes and indirect trans- 
mission seem the only basis of explanation (Figs. 124 and 311). 

There is a pseudohypersensitivity of enamel in some cases, due to 
apprehension. The patients can be ridiculed out of the idea by 
demonstrating its absurdity, as, for example, by touching a cusp 



HYPERSENSITIVITY OF DENTIN 311 

and then showing them the part touched. Pericemental irritability 
at times must also be excluded. 

There can be no question that systemic, nervous irritability from 
any cause aggravates the phenomenon of hypersensitivity, though 
whether it can make dentin more sensitive, or whether the patient 
is less able to endure pain, is not clear. 

The general perceptivity of the individual seems to play a part, 
and even apparently normal dentin may be exquisitely hypersen- 
sitive. Again, pain produced in excavation may be due to the 
character of the manipulation, heavy continued burring producing 
heat; lighter touches may excavate equally well, but produce much 
less pain. The dulness of the excavator or bur has a similar effect. 
The presence of some sensitivity of dentin on cutting is a positive 
sign of pulp vitality. 

The total absence of dentinal sensitivity should cause suspicion of 
pulp death but is not proof of it and further tests should be made. 

Diagnosis. — In the diagnosis the above characteristic symptoms 
are to be considered. The decisive test is made by pressing an 
instrument upon the suspected surface or cutting with a bur, when 
the characteristic pain is produced, subsiding upon or shortly after 
removal of the contact. 

Upon the pulpal wall of deep cavities doubt may exist as to whether 
the pain is due to pulp irritation. 

A suspected exposure may be differentiated by the localization of 
the pain upon touch, to a point corresponding to the pulp horn or 
pulp body, or by the point catching in the exposure. Hypersensitive 
dentin will be more generally distributed or occur at points at which 
exposure is impossible. Pulp abnormality or approach may be 
detected by means of a drop of cool water or a blast of cool air from 
a syringe, though this if obtained may generally be disregarded in 
shallow cavities. (See Hyperemia of the Pulp.) Dentin may react 
severely when fillings are pressed into even shallow cavities, some- 
times this is only momentary; occasionally the reaction continues for 
a time. Sometimes it causes a pulp hyperemia, usually passing away. 
Rarely the immediate reaction may be very severe necessitating the 
removal of the filling at once. Pain following drying may be dis- 
regarded as may that produced by the acid of cements. These 
remarks apply in cavities up to and including those classed as deeply 
seated. In case of almost exposed pulp the immediate reactions are 
more likely to be severe and the ultimate reactions are more likely to 
be pulpal. (See Arterial Hyperemia of Pulp.) 

Treatment. — The methods of treatment which have been followed 
for the relief of hypersensitivity of dentin, and the induction of such 



312 DENTAL CARIES 

a degree of analgesia as will permit the necessary cutting of dentin, 
may be divided into general and local. 

General Remedies. — The general remedies employed are those 
which abolish or lessen the perceptive function in the centers of the 
fifth pair of nerves, or which reduce hyperirritability of the nervous 
system. Either general anesthesia or general anodynes are em- 
ployed to lessen perception. The inhalation of a few whiffs of chloro- 
form or ethylic ether lessens the perception of pain, or a mixture of 
chloroform, ether, and alcohol may be used. Chloroform is usually 
avoided in this connection on account of its dangers when used in 
the sitting position. Slight etherization, the inhalation being carried 
only to the benumbing point, affords marked relief from the 
pain incidental to the cutting of hypersensitive dentin. While true 
it is rarely employed. Nitrous oxide and oxygen administered to 
the point at which "analgesia" without anesthesia occurs is a 
method now much employed. A special nasal inhaler admits the 
gases in various combinations, the mixture of the prepared gases 
being made in the mixing chamber of the apparatus, after the gases 
leave the cylinders. 1 

It is preferable that the gases be warmed to avoid the irritation 
of the lungs by the cold gases, though for short operations this is 
often omitted. 

Rebreathing the carbon dioxid and gases exhaled is also advocated 
as a respiratory stimulant and for economy. In view of hypersensi- 
tive dentin the method is now routine for cavity preparation and 
for the grinding of teeth with living pulps, for abutments or for other 
work involving a reasonable amount of pain. It is not generally 
useful for pulp removal unless complete anesthesia is induced. The 
method has various dangers which, while not preventing its use in 
careful hands, renders it not to be carelessly employed. Annoyances 
or occasional failure occur. Fear is apt to contra-indicate its use in 
children. 

The element of suggestion and confidence on the part of the 
operator seems to play an important part in the success of the anal- 
gesia, though the analgesia is not dependent upon it. The patient 
is able to cooperate with the operator, not having lost consciousness. 
In the practical application of the mixed gases, the apparatus is first 
set as to constancy of flow of both gases, the proportion of 95 per 
cent. N 2 and 5 per cent. O being first applied, until the patient 
reaches a condition of somnolence, of which he informs the operator. 
The proportions are now changed until approximately 80 per cent. 

1 For details of apparatus and application read C. K. Teter, Dental Cosmos, August 
1912; W. C. Teter, Dental Brief, August, 1911; A. E. Smith, Items of Interest, 
December, 1913; Harold B. Clark, Items of Interest, April, 1914, and others. 



HYPERSENSITIVITY OF DENTIN 313 

N 2 and 20 per cent. O are being given, though this proportion 
is variable. The patient is instructed to breathe through the nose if 
pain is felt, thus obtaining deeper analgesia. Conversely, as work is 
not being done, he may breathe through the mouth. If greater depth 
of anesthesia is required, the exhaling valve which ordinarily vents 
the expirations is adjusted and the patient then rebreathes the 
gases together with his own carbon dioxid, which further stimulates 
respiration, and gradually passes into anesthesia, especially if the 
percentage of oxygen be decreased. Without rebreathing, 95 per 
cent. N 2 and 5 per cent. will produce anesthesia. The amount of 
rebreathing is controlled by a valve and rebreathing bag. Somnoform 
(mainly ethyl chlorid) has also been used with a special inhaler 
(De Ford or Starck) to produce analgesia. 

The administration of general anodynes, particularly the com- 
bination of morphin and atropin, has been found useful in this field. 

1$ — Morphinae sulph gr. £ 

Atropinse sulph gr. t ±q 

M. et ft. pil. No. 1. 

Sig. — To be taken one-half hour before operation. 

Flagg noted that blondes bear morphin sulphate better than 
brunettes; particularly are nervobilious and bilionervous patients 
idiosyncratically opposed to its use, the physiological action of the 
drug being reversed or the after-effects being pronounced. Patients 
having dark hair and blue eyes may be expected to be thus idio- 
syncratic. For them, he recommended morphin bimeconate solution 
in doses equivalent to J grain of the salt, to be taken one the evening 
before, and the other before the operation. 

Chloral in 5 or 10 grain doses, administered in water before the 
operation, has a quieting effect upon the nervous system. Ambler 1 
has suggested the use of from 10 to 20 drops of fluidextract of piscidia 
erythrina, to be administered about ten minutes before operating. 
Drowsiness may be expected. Phenobromate, 10 grains, before 
operation, or 15 grains for any great pain, may be administered in a 
copious draught of water. 

For the reduction of excitement and nervousness in anticipation 
of dental operation, bromural, 5 grs., ordinarily to be administered 
while waiting, or 10 grs. in unusual cases, is highly recommended for 
this purpose by Hecker. 2 It is also useful in insomnia, and its 
associated hyperesthesia. Quinine sulphate, 5 grains a half-hour 
before operation, or better if preceded by another dose the day 
before it is to be used. The bromids, either of sodium, potassium or 
ammonium or triple bromid, may be taken the day previous' and just 
before coming to the office. The dose may be from 5 to 15 grains. 

1 Dental Cosmos., 1901. 2 ibid., 1909. p. 844. 



314 DENTAL GAMES 

Hyoscyamin hydrobromate, eV grain, will be useful in those cases 
which are associated with muscular spasm or hysteria. 

The coal-tar derivatives, phenacetin, acetanilid, and others, are 
occasionally efficient. The preparation known as antikamnia (said 
to be a combination of acetanilid, caffein citrate, and sodium bicar- 
bonate) and ammonol (acetanilid and ammonium carbonate, equal 
parts) are to be preferred in this connection. The dose of the latter 
two is 10 grains, administered one-half hour before operation. 

The writer has one patient who obtains a sufficient analgesia for the 
excavation of very sensitive cavities by taking small doses of whisky. 
Rapid breathing until the "head swims" according to Bonwill's plan 
has been of use in some cases. 

The induction of the hypnotic state belongs in the category of 
means acting upon the nerve centers. The use of the ordinary sug- 
gestion that the work will not be unduly painful, considerate treat- 
ment, patience, and the employment of remedies all have a calming 
influence, permitting relaxation upon the part of the patient, who, 
if "keyed up" to expect great pain, will expect and feel unduly. 

Conductive Anesthesia. — Midway between truly systemic and 
purely local measures lies the method of anesthetizing the nerve tract 
leading from a tooth to the brain. This is truly a "nerve blocking" 
in which the nerve is rendered incapable of performing its function 
of sensation. Two methods are employed: (1) An injection into gum 
tissue intended to cause the anesthetic to reach the sensory nerve in 
the apical tissue after passage through the bone. This is called from 
the site of injection "mucous anesthesia" also "infiltration anesthesia." 

2. When the injection is made at some more distant portion of the 
nerve (along the course of its main trunk) it is called "conductive 
anesthesia," though the term "nerve blocking" would be just as 
applicable. It is plain that there is no distinction in principle in any 
of the forms of local anesthesia. It is simply a question of the site 
of application, pulp, apical nerve or nerve trunk; in all a temporary 
sensory paralysis is produced. When the hypodermic or deep injec- 
tions are made the following conditions are necessary: 

1. A competent armamentarium. 

2. Complete asepsis. 

3. An effective, safe and isotonic anesthetic solution. 

4. Correct technic, which involves a knowledge of the anatomy 

of the part. 

5. A sufficient allowance of time for infiltration of the anesthetic. 
1. The necessary special instruments are a sterilizable syringe, 

all metal, Fischer, Tagg Record, etc., a short iridio-platinum needle 
(23 mm.) and a long one (42 mm.) (Fig. 316.) These are to be kept 
in good order and should never be used if they leak back around the 



HYPERSENSITIVITY OF DENTIN 



315 



Fig. 316 



plunger. All hubs and needles should fit tightly and not leak under 
considerable pressure. For conductive anesthesia iridio-platinum 
needles are used; but, if preferred, steel needles may be used, but 
require more time for care, which increases 
the eventual cost, and they have disadvan- 
tage in that they cannot be flamed, and are 
said to break more readily. In mucous 
anesthesia the tough gum tissue renders 
fine, short, steel needles advisable (28 
gauge, I inch). The hub provided shortens 
the needle exposed to a correct length for 
each form of anesthesia. 

2. Asepsis is maintainable by glowing 
the platinum needle in a Bunsen or alcohol 
flame before and after the injection, keep- 
ing the mounted syringe and extra needle 
in an antiseptic solution (alcohol 2 parts, 
glycerin 1 part) in an air-tight jar or a 
large Petri dish. When using, place syringe 
under the hot water tap to wash off the 
alcohol; dip in the sterilizer containing 
boiling distilled water and draw it full of 
the water and eject three times to clear 
the interior. The needle is then flamed 
and the anesthetic solution drawn in. The 
syringe is then placed in the folds of an 
aseptic towel and the needle should touch 
nothing until the injection is made. The 
field of operation is wiped off and gently 
scrubbed with iodin tincture (for alterna- 
tive see Asepsis) and the hands are to be 
sterilized (see Aepsis). Blum 1 suggests as a 
local analgesic and antiseptic a solution 
containing equal parts of tincture of aconite 
and iodin and absolute alcohol. The solu- 
tion is considered later. 

3. For extractions done often each day 
a special solution may be made for a suitable period (see works on 
dental materia medica). For the present purposes the solution is 
now usually made as needed from a tablet (E) of novocain suprarenin. 

1$ — Novocain 0.02 gram 

Synthetic suprarenin 0.00005 gram 

"Procaine" is the official name of the U. S. Government for para-amino-benzyl- 
diethyl-amino-ethanol formerly made in Germany as novocain and identical with it. 




Syringe mounted with 
Schimmel hub C and 42 mm. 
needle for injection at infra- 
orbital foramen and mandib- 
ular foramen. (Fischer.) 



1 Items of interest, 1915, p. 648. 



316 



DENTAL CARIES 



This keeps indefinitely, though spoiled if found pink in color. (Tablet 
T contains less suprarenin.) This is added to 1 mil. (c.c.) of the follow- 
ing solvent and vehicle: 

1} — Calcium chlorid . 04 gram 

Potassium chlorid 0.02 " 

Sodium chlorid . 05 " 

Distilled water (sterile) 100.0 mils. (c.c. or grams) 

This makes 1 mil. (c.c.) of a 2 per cent, solution, therefore one 
tablet should be added to each mil. of solvent to make the desired 
quantity. To make a 1 per cent, solution add one "E" tablet to 
each 2 mils, of solvent and for a 1.5 per cent, solution add one to 
each 1.5 mil. of solvent. 

Fig. 317 




Posterior view of position of needle in mandibular anesthesia: 1, external oblique 
line; 2, internal oblique line; 8, position of needle at superior margin of lingula; 4, 
most suitable length of needle behind lingula (a further advancement would result in 
failure); 6, position of needle, 1 cm. above level of masticating surfaces of molars; 7, 
lingula; 8, inferior dental foramen. (Fischer.) 



Fischer claims that the calcium chlorid acts as a heart activator 
and offers evidence in proof of its value as against a sterile physio- 
logical sodium chlorid solution alone which, however, may be used 1 
and is advised by Prinz. The above solvent may be prepared from 
purchasable "Ringer tablets," one being added to each 10 mils, of 
sterile distilled water and the whole boiled for ten to twenty minutes 
in the dropper bottle (with cotton in the mouth) by setting on a cloth 
in boiling water in a pan. The dropping bottle ma}' be kept practi- 



Journal of Allied Dental Societies, September, 1914, p. 416. 



HYPERSENSITIVITY OF DENTIN 317 

cally sterile by inverting a small measuring glass over it and placing 
over the whole a bell jar or a "cozy." 

When making up the anesthetic solution, drop the required amount 
into a porcelain "Novocain dissolver" which is graduated in mils., 
boil and add the required number of E tablets and gently heat again 
until dissolved. It is placed in the fold of the aseptic towel until the 
syringe is prepared. The order may be reversed. The stock bottle 
of distilled water should have its stopper and neck covered with a 
wad of cotton held by a rubber band. It is wise to occasionally boil 
it. Usually 2 mils, of solution suffice for even conductive anesthesia. 
Fischer 1 places 20 mils, of a 2 per cent, solution as the maximum 
dosage, but states that in surgery 200 mils, of a 1.5 per cent, solution 
has been used in Europe with impunity. It would be wise to keep 
well within Fischer's figures, at say two "E" tablets at one sitting. 
When mucous anesthesia is employed, the solution is injected into 
and beneath £he periosteum, both buccally and lingually, as nearly 
over the apex of the root as possible and gently massaged into the 
bone. For single-rooted teeth a buccal injection may be sufficient. 
The 25-m. needle is employed. About ten minutes are required to 
produce satisfactory pulp anesthesia. Fischer 2 emphasizes the follow- 
ing conditions for success in mucous anesthesia: 

1. The application of a stasis bandage slightly compressing the 
carotid artery and the veins of the neck, to help retain the anesthetic, 
and prevent cerebral anemia. 

2. The periosteum, not the submucous tissue must be infiltrated. 

3. One injection to be made on each side of the teeth. The fewer 
injections the better the effect. 

4. The part must be sterilized with tincture of iodin and the 
sterile needle must have its orifice faced toward the bone. 

5. Slow, moderately strong pressure during the injection. 

6. The point of injection must be compressed with the finger, 
after the needle is withdrawn to allow diffusion of the anesthetic. 

In conductive anesthesia, the anesthetic is injected into the tissue 
contiguous to a nerve trunk. The technic for upper second bicuspid 
to third molar controlled by the posterior superior dental branches 
of the second division of the fifth nerve (known as the maxillary 
tuberosity injection), is as follows: 

Palpate the molar process with mouth half open with the fore- 
finger and raise the cheek with it and the thumb. Insert the 42-mm. 
needle with the opening toward the bone into the loose tissue at 
the reflex of the mucous membrane just posterior to the root of the 

1 Journal of Allied Dental Societies, 1914, p. 420 ; 

2 Local Anesthesia in Dentistry. 



318 



DENTAL CARIES 



upper first molar Fig. 318-£. Follow the surface of the bone through 
loose tissue at an angle of about 45 degrees upward and backward 
until the needle is inserted to the hub. Injection is made in one of 
two ways: 

1. Just after penetration by the needle a portion of solution is 
injected and the injection repeated as the needle is advanced. 

2. The better method, allowing the pen grasp of the syringe through- 
out, is to insert the needle to its full depth as. this is practically pain- 
less after the mucosa has been penetrated. Injection of half of the 





Fig. 318 








_ 








; — — v;-~ 


j 




■ ' P 


{ 


JZ&t 




i 


¥&"-■ 








Om 





Prints of injection in the maxilla in mucous and conductive anesthesia. U, line of 
reflection cf mucous membrane: 1, injection tor upper right central incisor; 2, for 
upper right lateral incisor; 3, for conductive anesthesia cf upper right lateral, canine, 
and first bicuspid, the needle to be advanced to the infraorbital foramen; 4, for up- 
per right second bicuspid; 5, for upper right first molar; 6, conductive anethesia at 
maxillary tuberosity for upper right first, second, and third molars; 7, conductive 
anesthesia for upper right third molar. (Fischer.) 



2 c.c. of solution in the syringe is then made for the higher branch 
(Fig. 318-frr) and the syringe partly withdrawn and the balance in- 
jected for the lower branches. This injection suffices for pulp and 
dentin work. For extractions an injection must be made about 
one-half inch above the gingival margin of the third molar into the 
palatal mucosa and to the periosteum to infiltrate the anterior 
palatine nerve Fig. 319. Ten minutes is about the waiting period. 

Technic for Upper Central Incisor to First Bicuspid (known as 
the infraorbital injection.) This region is controlled by branches 
from the infraorbital nerve which must be anesthetized just within 
the border of the infraorbital foramen. To do this place the fore- 
finger at the inner canthus of the eye ; draw it down and outward 



HYPERSENSITIVITY OF DENTIN 



319 



along the border of the orbit to a point 0.5 cm. below it and about 
the same distance from the border of the malar process. This spot 
is somewhat more sensitive than others. It should then be almost 
directly over the first bicuspid and be upon the location of the infra- 
orbital foramen. The lip is raised with the thumb and the needle 
inserted somewhat away from the bone into the mucosa reflex 
just posterior to the cuspid tooth. It should penetrate to a point 

Fig. 319 




Posterior pal- 
atine fora- 
men 



"^J~f 



Bony surface of palate. The crosses indicate the points of injection fcr mucous 
anesthesia; those at the palatal of the third molars are the sites for blocking of the 
anterior palatine nerve for extractions and surgery of alveoli; for blocking cf naso- 
palatine nerve inject one-fourth inch above the lateral incisor of respective side. 
(Fischer.) 



just beneath the finger tip. Somewhat forcible injection is then 
made beneath the finger and from 0.5 to 1 c.c. of solution is 
injected and well massaged into the foramen to anesthetize the 
anterior superior dental nerves. This serves for pulp and dentin 
work, but for extraction an injection must be made one-quarter 
inch above the gingival margin of the lateral of the respective side 
to infiltrate the naso-palatine nerve at the neighborhood of its 
foramen (Scarpa's). Ten minutes is the waiting period. 



320 DENTAL CARIES 

Technic for the Mandibular Injection. — This accomplishes anes- 
thesia of the pulps of teeth, the bone and mucous membrane of 
one side of the mandible by infiltration of the inferior dental branch 
of the fifth nerve at its entrance into the inferior dental canal and 
by infiltration of the lingual nerve at a point anterior to the location. 
One injection only need be made for pulp and extraction work. Between 
the internal oblique line of the ramus and the external oblique line and 
back of the last molar lies a grooved depression known as the retro- 
molar triangle (Fig. 317-6") . This should be palpated from the front on 
the right side and from around the head on the left side with the tip 
of the left forefinger. The nail should lie at the internal oblique line. 
The middle of the finger-nail is the landmark for insertion of the 
needle. The syringe barrel is laid across the contact between the 
canine and first bicuspid of the opposite side and the needle inserted 
close to the edge and needle of the finger-nail. Some prefer to 
enter straight, find the internal oblique line and pass it, then 
to throw the syringe to the opposite side. This should be about 
1 cm. above the occlusal of the last molar. The needle is inserted 
into the mucosa, carried to the bone and then with a minute 
withdrawal to escape the periosteum is carried along the soft tissue 
close to the bone and yet away from periosteum. If the needle 
catch a protuberance it should be slightly withdrawn and carefully 
advanced around it (this to avoid breaking the needle). This general 
mode of advance is made until the needle is one-fourth inserted, 
when a small portion of solution is deposited for anesthesia of the 
lingual nerve. The advance is then continued to the full depth 
to the hub of the 42 mm. needle (about 25 mm. of needle). The 
needle point then lies in a safe position in the region near the nerve 
(Fig. 317-4). Changing the hand to the injecting position the balance 
of the solution is injected. From ten to twenty minutes is the 
waiting period for the mandibular injection. Occasionally a mucous 
anesthesia is required over the special tooth. 

While the time required for anesthesia is about ten minutes in 
the maxilla and twenty in the mandible, one may test with a bur 
(or lancet on the gum) for a satisfactory result before this time. 
Occasionally a pulp is not anesthetized at all while other tissues 
seem to be and occasionally an apical portion only is sensitive. 
The writer when having a tooth extracted distinctly felt the burn 
of iodine applied to the gum margins while the extraction was painless. 
These peculiarities have not been explained. 1 

1 Theodor Blum has an excellent article in Items of Interest, 1908, p. 181; also 
Dental Cosmos, April, 1919. 



HYPERSENSITIVITY OF DENTIN 321 

Other Considerations: Rapid beating of the heart is variously 
said to be due to the suprarenin, while Silverman 1 claims it occurs 
when novocain only is used. The writer finds it as well as any 
faintness, which is rare, to be rapidly amenable to aromatic spirits 
of ammonia. Camphorated validol is also recommended by Reith- 
miiller. These or bromural may be given in advance to nervous 
patients. Anesthetics should not be injected into septic areas, 
especially abscesses, as toxins or bacteria may be forced into the 
blood or adjacent parts. Some claim that this is the cause of any 
toxic symptoms which may later be produced, but the author had 
one such case in which the patient left the office apparently normal 
but had to be helped home from the street car, and there was given 
coffee liberally. The injection was aseptically made into healthy 
gum tissue on both sides of a bicuspid for pulp extraction. In another 
case, in which one-third grain only of procain was used for a mucous 
anesthesia in healthy tissue near a pyorrhea pocket, before the oper- 
ation could be done the patient was faint and vomited. Silverman 
advises a slow injection occupying a full minute. As erotic symp- 
toms are said to occur there should be a third party present as in 
general anesthesia. 

Both mucous and conductive anesthesia are warrantable procedures 
and should be resorted to in preference to long-continued treat- 
ment of cases by other methods. They are of value in all cases of 
dentin, pulp, gingival, pericemental or bone disease in which opera- 
tion would be unduly painful. Nevertheless the writer does not use 
them constantly for ordinary cases of excavation, pyorrhea treat- 
ment, etc. 

In case a needle break off in the tissue it should be removed as 
it may migrate and cause trouble. The tissue being anesthetized 
if the injection has been made, or specially anesthetized if this was 
not done, it is rational to make a cut as nearly at right angles to the 
needle as may be and deep enough to feel its mesial end. The 
edges of the cut are retracted and the needle grasped and removed 
with suitable forceps. Berger 1 describes such an operation. 

In apicoectomy conductive anesthesia should be fortified by mucous 
anesthesia, and for upper anterior teeth Peck's method of packing the 
anterior nares with cotton and a 20 per cent, solution of novocain is 
advocated by Prinz. 2 

Mucous or Infiltration Anesthesia. — This is a form of conduc- 
tive anesthesia (as related to this subject) in which injection of a local 
anesthetic is made beneath the periosteum on one or both sides of 

1 Items of Interest, September, 1915, p. 660. 

2 Dental Ccsmos, May, 1918, p. 386. 
21 



322 DENTAL CARIES 

the alveolar process in such situation as to infiltrate the apical 
tissue and the branch of the fifth nerve leading from the pulp. The 
short needle is used, its orifice facing the bone, and is introduced at 
a point as nearly over the apex as possible. The finger is placed 
over it and a slow forcible injection made with endeavor to massage 
the solution toward the apical tissue. The results are best when 
the solution does not escape into soft tissues, which may largely be 
prevented by finger pressure higher up. No good effect upon dentin 
is noted unless the apical tissue is infiltrated. When accomplished 
even a pulp removal can be done. 

For extraction the aim is to anesthetize the pericementum and 
gum tissue and the injection is made on both sides of the alveolar 
process. 

Diploic ok Intraosseous Anesthesia. — For deep anesthesia about 
a molar, the; gum may be anesthetized and a cut made to the bone, 
a small sterile drill is then driven through to the cancellated structure. 
A further injection is then made with a blunt needle, such as is used 
in high pressure work. This operation has been modified by the use 
of a needle constructed to simply indent the cortical layer of bone, so 
that the force of the plunger may cause the direct infiltration of the 
apical tissue. This uses the principle of high pressure anesthesia 
as applied to dentin. 

While the operation of diploic anesthesia seems heroic, there is 
no good reason for so regarding either this or the operation of conduc- 
tive anesthesia in general as more dangerous than ordinary mucous 
injection. The rule of safety lies in knowledge of anatomy, safe 
dosage, and sterility — in short, in correct technique. 

The introduction of a 5 or 10 per cent, solution of cocain upon 
cotton into the nostril, upon the side of operation, is endorsed by 
Peck, of Chicago, as a means of anesthetizing the nerve trunk 
leading from the upper incisors. Escat, of Toulouse, France, has 
observed that a 0.1 per cent, solution on cotton about the size of an 
almond, placed in the nostril in close proximity to the anterior edge 
of the inferior turbinate, will in twenty minutes anesthetize the 
anterior superior dental branch of the fifth nerve, which lies in close 
proximity to the nasal mucous membrane at this point. The entire 
tissue about the incisors and cuspids of the side is anesthetized, as 
is sometimes that of the opposite side in part. 

Reflex Anesthesia. — Claims are made by Dr. William H. 
Fitzgerald, M.D., that pressure with a metal probe tipped with 
cotton upon certain parts of the mouth and fingers, will produce 
satisfactory oral anesthesia and even of more distant parts. Cura- 



HYPERSENSITIVITY OF DENTIN 323 

tive effects in certain body diseases by proper manipulation are 
claimed. The method has not obtained any vogue. 1 

Local Treatment. — The local treatment of hypersensitive dentin 
may be considered from two standpoints, according to whether a 
concavity containing it requires excavation, or whether the hyper- 
sensitive spots are not to be excavated after treatment. 

Treatment in Cavities of Decay. — The remedies employed in 
the endeavor to reduce or abolish hypersensitivity in a cavity of 
decay at the time of operation are quite numerous; few are, however, 
always effective. They may be classed under two headings : 

1 . Those which temporarily benumb or anesthetize the fibrillse and 
prevent the transmission of sensation. 

2. Those which chemically destroy the fibrillse for a distance, thus 
preventing transmission of sensation. 

Remedies which Benumb the Fibrillse. — Chief among these 
for its universality of application is dryness. Dentin, which protests 
against even the touch of an instrument while wet, has its sensitivity 
so lessened after the application of a rubber dam and drying, that it 
may be cut freely, in many cases without the aid of medicinal agents. 
So well is this recognized that isolation and drying of teeth are 
regarded as a necessary preliminary to cavity preparation. The 
degree of insensitivity induced is in proportion to the dryness. The 
drying temporarily deprives the dentinal protoplasm of a portion of 
its water, and inhibits the transmission of sensation by reducing 
functional activity. 

A continuous but gentle blast of air, passed from a compressed-air 
apparatus or double bulb through a heated metal bulb and nozzle, 
or through an electrically heated coil, should be employed until the 
dentin is desiccated. This is evidenced by its extreme whiteness. 
Other forms of hot-air syringes may be substituted with less satis- 
faction and greater fatigue to the operator. The double bulb may 
be operated by the patient. 

The application of absolute alcohol assists the drying because of 
its affinity for water. The addition of a little menthol to the alcohol 
assists by anesthetic action. The pain from the warm air may at 
first be quite severe, but even in greatly hypersensitive cases the 
nozzle of the syringe may soon be approximated to the cavity, though 
in some cases it may be necessary to make an application of a mixture 
of equal parts of carbolic acid and oil of cloves, or of gum camphor 
and carbolic acid (phenol camphor), both of which have some 

1 Items of Interest, March, 1915. 



324 DENTAL CARIES 

anesthetic effect. Menthol may be added to either. When desirable, 
their effect may be hastened by pressure with unvulcanized rubber. 

An instrument known as the "dehydrator" causes absolute alcohol 
placed in a special chamber between the bulb of the hot-air syringe 
and the nozzle to be vaporized upon the hypersensitive dentin. 
The drying effect is thereby augmented and the dentin satisfactorily 
obtunded. Natural dryness obtained by applying rubber dam, mod- 
erate drying with warm air and allowing the patient to wait approxi- 
mately an hour has been very effective in extreme cases. 1 

Some degree of dryness is, as a rule, a necessary preliminary to 
success with other applications. 

Following dryness, the excavation should be done with sharp 
instruments and burs. The latter should only be lightly touched to 
the dentin and be revolved at high speed. Letting the bur occa- 
sionally run free cools it. The heat of friction is considerable and 
highly irritating. 

The combination of potassium carbonate with glycerin makes a 
water-extracting combination having but little coagulating power. 
For this reason it may be used in the deeper cavities, but not in cases 
of almost exposed pulp, as in such cases its application is painful. 

1$ — Potassium carbonate gr. xv 

Glycerin f5J 

Mix in a mortar. 

To be applied on a pellet of cotton. (Flagg.) 

It may be used with effect even upon slightly moist dentin. 

Not being escharotic to the gum, this remedy is exceedingly useful 
about the sensitive but undecayed necks of teeth, and may be freely 
applied after moderate drying of the parts. 

If necessary, the patient may be given the prescription and directed 
to apply by means of a clean tooth-pick, which should not be used 
a second time, as the mixture may be infected and spoiled. 

The part is dried with a bit of clean cloth and the material applied. 
The mouth is kept open until the pain ceases. 

Its pain simulates that of zinc chlorid, but is less severe in its 
character. 

A mixture of tannin and glycerin has a similar effect. 

3 — Tannin 5J or 3ij 

Glycerin fgj 

Mix in a warm mortar. 

Zinc chlorid by its affinity for water also acts in this manner, but 
being also a caustic it is described with the next class. 

1 Guilford, lecture. 



HYPERSENSITIVITY OF DENTIN 325 

Hot water supplied by a tube leading from a coil heated by 
electricity and attached to the water supply pipe of the fountain 
cuspidor has been recommended by A. F. Merriman, Jr., for the 
obtunding of hypersensitive dentin in cases in which dryness is not 
readily obtainable, nor immediately or subsequently desirable. 

It is claimed that satisfactory analgesia is obtained, and that the 
mucous membrane of the mouth is not unduly uncomfortable, even 
when the heat is objectionable to the finger of the operator. The 
advantages of the method for excavation and grinding are obvious 
and most useful, particularly for trimming live teeth. A spray of 
blood-warm water from an atomizer operated by compressed air may 
be used with the bar or stone with satisfaction. 

Buckley 1 has recommended: 

1$ — Mentholis gr. xx 

Chloroformi f^ij 

Etheris . qs. ad. fgjM. 

Sig. — Place a little on cotton in the cavity after the rubber dam is adjusted and 
evaporate to dryness. 

Refrigeration by a spray of ether or ethyl or methyl chlorid reduces 
the temperature of the fibrils and pulp, benumbing them. The 
rubber dam should be applied to isolate the teeth operated upon. 
Ether and Rhigolene are applied by means of a double-bulbed 
atomizer, or one operated by compressed air; the chlorids are 
contained in glass tubes conveniently capped wliich conserve the 
preparation. The cap being raised, the heat of the hand causes 
vaporization of the agent within the tube, which forces the liquid 
out of the orifice of the tube in a fine but forcible stream. A spraying 
nozzle is also obtainable. The cavity should at first contain a pellet 
of cotton, in order that the dentin may be gradually obtunded and 
painful response on the part of the pulp avoided. The method may 
be painful in application, but often satisfactory. Ether odorizes the 
operating room, and a flame must be avoided. 

"Vapocain" and "potassocain," proprietary agents which consist 
of a 15 per cent, solution of cocain in ether, are applied to hyper- 
sensitive dentin upon the theory that the ether enters the tubules, 
carrying the cocain into contact with the fibrils; the ether evapo- 
rates, leaving the cocain in aqueous solution to benumb them. This 
requires several minutes. They are useful in the deeper cavities. 
Jack recommended that the cavity acidity be neutralized before their 
application. 2 

1 Dental Cosmos, August, 1907, p. 328. 

2 American Text-book of Operative Dentistry. 



326 DENTAL CARIES 

A 10 to 25 per cent, solution of cocain hydrochloride or novocain 
in water may be forced into the tubules by applying it on a pellet of 
amadou, placing over this soft vulcanite rubber, and producing 
pressure with a burnisher for from three to six minutes. The pressure 
should be gradually applied. A gratifying degree of dentinal anes- 
thesia may often be obtained. 

Adrenalin chlorid solution, 1 to 1000, plus chloreton 1 or cocain, 
has been used in this manner with some effect. A few crystals of 
the cocain or novocain may be picked up on a pellet of cotton moist- 
ened with warm water and pressed upon the cavity surface. 

Fig. 320 




Ethyl chlorid spray tube. 

Buckley 2 recommends spreading cocain alkaloid made into a 
creamy paste with liquid petroleum or oleate of cocain over the 
surface of cavities in children's teeth and sealing for a day or two. 

Miller 3 has shown that by taking a modelling composition impres- 
sion of the cavity, then applying a few threads of cotton saturated 
with cocain to the floor of the cavity, then placing a thickness of 
rubber dam over the entire cavity surface, replacing the modelling 
composition, and producing pressure, anesthesia can be produced 
when there is not a greasy condition of the cavity, nor thick layers of 
decalcified dentin nor much secondary dentin present. 

Soderberg 4 has shown that painless excavation of cavities other- 
wise uncontrollable may be effected by the use of nervocidin, an 
alkaloid obtained by Dr. D. Dalma from the East Indian plant 
gasu-basu. Twenty-four hours are required for complete dentinal 
anesthesia without pulp anesthesia unless a second application be 
made. 

The primary effect of nervocidin being irritating, Soderberg recom- 
mends the additional use of cocain, both being mixed with zinc 
sulphate cement. 

1 Parke, Davis & Co. 2 Johnson's Operative Dentistry 

3 Dental Review, 1906. 4 Dental Cosmos, August, 1903. 



HYPERSENSITIVITY OP DENTIN 327 

1$ — Gum arabic 3J 

Zinc sulphate 5ss 

Water f 5 j — M. 

Dissolve the zinc sulphate in the water, add the gum arabic, stir; let stand for 
twenty-four hours and strain. 

1$ — Of above solution f3ij 

Nervocidin gr. x 

Cocain hydrochlorid gr. x — M. 

To a portion of the latter solution add uncalcined zinc oxid to 
make a cement, which is placed in the dried cavity. Uncalcined zinc 
oxid added to the first formula makes zinc sulphate cement. After 
excavation the acidity of the nervocidin should be neutralized. 

Cataphoresis (Greek kata, down, and phoreo, I bear or bring) is, 
in technical parlance, the transference of substances from the anodal 
or positive pole of a battery toward the cathodal or negative pole. 
They are thus carried into the tissues. 

Cataphoresis is to be distinguished from electrolysis, by which 
substances are decomposed and their elements carried from positive 
to negative or from negative to positive poles, according to their 
polarity. In cataphoresis a substance is carried unchanged from the 
positive toward the negative pole, after the manner of granules in 
protoplasm acted upon by the same force. 

The conduction of cocain from + to — poles, that is, in one 
direction only, in this manner, has been questioned by Sturridge, 
who is of the opinion that the cocain dissolved in water is split 
into ions (in this case minute fragmented particles of molecules 
with an equal number of + and — ions each conducting electricity 
and travelling in opposite directions to their respective (opposite) 
poles). In this case only the positively electrically charged ions 
will travel toward the negative (the hand) into the pulp. There is 
a further possible view of which there is no evidence of which the 
writer is aware, that the cocain is electrolyzed, the resulting ions 
which have anesthetizing power being conveyed into the fibrils or pulp 
tissue. 

As applied to dentistry, a primary current from a battery capable 
of delivering from 30 to 40 volts has the positive pole or conductor 
connected with a resistance or current controller, capable of being 
so manipulated as to gradually reduce the resistance to the current a 
fraction of a volt at a time. This is called a " fractional volt selector." 
This is usually a "broken ring" of graphite, to one end of which the 
positive current is admitted by means of the conducting cord and 
travelling indicator; at the other end the current passes out by a 
similar cord, which in turn is attached to a milliamperemeter, or 
instrument recording the quantity of current passing through the 



328 DENTAL CARIES 

circuit. From this a cord leads to the positive electrode applied to 
the tooth cavity. To the face, neck, or wrist of the patient a moist 
electrode (negative) is applied, which by its conducting cord leads 
the current back to the negative or zinc pole of the battery. The 
current passes in turn from the battery through the resistance, 
milliamperemeter, dentinal fibrils, pulp, arm, hand, to the battery. 

The milliamperemeter is a convenient but not an essential feature 
of the apparatus, and as a volt-selector, a rod of graphite or a glass 
tube with water resistance may be used. Fig. 321 shows the more 
elegant apparatus arranged almost as described. An ionizing appa- 
ratus is constructed upon exactly the same principles and they are 
therefore interchangeable. 

In the use of the cataphoric apparatus, the tooth is securely in- 
sulated by well-ligated rubber dam and cotton saturated with a 
solution of cocain hydrochlorid or citrate, of a strength of from 10 
per cent, to a saturated solution is placed in the cavity. The platinum 
anode is wrapped with cotton, dipped in the solution, and inserted 
into contact with the cotton in the cavity. The controller is now so 
manipulated as to gradually cut out its resistance to the current. 
When pain is felt the controller is turned back slightly until it passes 
and then again advanced. The high resistance of the dentin is gradu- 
ally overcome. 

The cocain solution should be renewed as dryness occurs, as dryness 
increases the resistance. The cocain is carried along the fibrils to 
the pulp by the electric current, and dentinal, followed by pulpal 
anesthesia results. 

From eight to fifteen minutes, or sometimes longer, are required 
for dentinal anesthesia, which loss of time is largely regained in the 
facility of operation. 1 

Price 2 has shown that pulp anesthesia is gained more readily by 
concentrating the action of the cocain upon the pulpal wall by means 
of a small electrode. If general dentinal anesthesia is required he 
prefers this method, as the pain receptivity of the pulp is abolished. 
A broader application anesthetizes the dentin. 

Woodward 3 has shown that in the latter case the dentin in a cavity 
upon the opposite side of a tooth being operated upon, may remain 
sensitive. This indicates that the pulp bulb has not been entirely 
anesthetized and is about the best point to which to advance the 
anesthesia. 

The pulp is not injuriously affected in ordinary applications, unless 

1 Jack: American Text-book of Operative Dentistry. 2 Dental Summary, April. 1903. 
3 International Dental Journal, November, 1902. 



HYPERSENSITIVITY OF DENTIN 329 

saturated by long application. A reaction resulting in hyperemia may 
take place. To obviate this, the pulp should not be oversaturated, the 

Fig. 321 




S. S. White cataphoric outfit. The connections with the patient are not in the 
illustration. The small electrode is the one applied to the tooth; the larger is for the 
hand. The direction of current will depend upon the connections at the battery. 



330 



DENTAL CAUIES 



fibrils should be treated with carbolic acid, and in deep cavities a 
thermal non-conductor should be used before filling. 

In case absolute insensitivity is produced, the anatomy of the pulp 
must carefully be considered, so that it be not exposed during the 
excavation of the cavity. This can be determined by instrumental 
examination. 

The pulp may have cocain or novocain forced into it by means of 
a powerful compound-pressure syringe. The Meyers syringe is one 
of the best. It is filled with a 2 per cent, solution of cocain or novocain 
in Ringer or salt solution. A convenient drill pit is made with a 
No. i bur; this may at first be but part way through the enamel if 
necessary, usually it is made in the dentin; the tapered nozzle of the 
filled syringe freed of air is forced into the opening and continuous or 
intermittent pressure produced without releasing the point for several 
minutes. It is well to allow the air to escape from the pit by holding 

Fig. 322 




The Meyers compound syringe for forcing cocain solutions through the dentinal 

tubules. 



loosely for a moment. If the pit is made in the enamel only such time 
as required to deepen it painlessly need be given (twenty to sixty 
seconds). If preferred the needle may have a flat end and the drill 
pit be made with a cone-shaped bur. The object is a tight-fitting 
joint as leakage causes failure of force. An average of about three 
minutes will be required for sufficient infiltration of the pulp. There 
are occasional failures in this method. No general cavity anesthesia 
will result until the solution has infiltrated the area of pulp underlying 
the fibrillar connections with the pulp. The forcing of cocain into so 
delicate a tissue should stop at that point, unless pulp removal is in- 
tended, as more may produce expansive pressure, and may cause a later 
pulp reaction, as cocain is, to a degree, a protoplasmic poison. It should 
be so injected into only sound dentin or enamel. If the cervix of a 
cavity is used as the point of injection, the pit should be made deeper 
than the syringe nozzle penetrates, as in this way the lateral tubules 
can carry the cocain, otherwise they may be occluded by the syringe 



HYPERSENSITIVITY OF DENTIN 331 

point. Ingalls 1 has devised a syringe in which the force is applied by 
compressed air. Secondary dentin is difficult of penetration, and 
gradual approaches must be made. The method is useful in pulp 
extirpation rather than in hypersensitivity, but has occasional use, 
especially in cervical cavities. 

Remedies which Chemically Destroy the Fibrils for a 
Distance, Preventing Transmission of Sensation. — Agents 
which chemically destroy the dentinal protoplasm form the most 
extensive group of dentinal obtundents. They include salts of 
metals, such as zinc chlorid and silver nitrate; carbolic acid and its 
derivatives, and like bodies; the cresols, etc.; mineral acids, notably 
sulphuric, chromic, and nitric; organic acids — trichloracetic and lactic 
acids — (full strength) ; alkalies — sodium and potassium hydrates and 
carbonates. 

Zinc chlorid, silver nitrate, and carbolic acid all cause coagulation 
of the fibrils of the dentin. The mineral and organic acids chemic- 
ally decompose both protoplasm and the calcified tissues. The 
concentrated alkalies chemically destroy protoplasm and bring 
about its quick dissolution. Like all active chemical substances, the 
extent of their action depends upon the freedom with which they 
are applied. 

The application of any of these agents, as a rule, causes pain, the 
degree of suffering being usually in proportion to the depth of the 
cavity. For this reason the more powerful agents, like zinc chlorid 
and nitric acid, are to be confined to cavities of moderate depth, 
while carbolic acid, especially in combination with the oil of cloves, 
may be used in the deeper ones. 

Fused zinc chlorid is used in its deliquesced form, and is most 
active when some of the salt is still undissolved in the bottle. Its 
pain in suitable cavities is a full, bearable one, gradually increasing, 
sometimes in waves, until a crisis is reached, when the pain gradually 
ceases. It has a double action, not only coagulating protoplasm, 
but combining with its water, owing to its affinity for the latter. 
On account of this property its action may be limited by warm water. 

An undue action of the zinc chlorid is indicated by a throbbing 
pain; this indicates that the pulp has been irritated. When, as occa- 
sionally occurs, no pain is produced, no obtundent effect is obtained. 
If this occur regularly the drug is oversaturated with water. 

Bogue has suggested that cocain crystals be incorporated with 
the chlorid of zinc as a means of alleviating the pain incident to the 
application. 

1 Items of Interest, January 1916. 



332 DENTAL CARIES 

Miller, following Hoffheinz, advocated the use of equal parts of 
zinc chlorid and chloroform. 

Buckley modified this by using the following: 

R- — Zinc chlorid gr. xx 

Alcohol f5iv 

Chloroform f$j — M. 

Apply on cotton gently evaporate to dryness. 

Certain moderately deep cavities may be filled with oxy chlorid of 
zinc cement, the free zinc chlorid acting as an obtundent. This 
requires a prolonged action, and is only resorted to in cases which 
do not admit of immediate work, or in which procrastination is 
desirable. 

A formula of wide renown is known as Robinson's remedy; this 
may be made in one of two ways: 

R — Potassium hydrate 

(or Sodium hydrate), 

Carbolic acid p. aeq. — M. 

Reduce the gelatinous mass formed with alcohol. 

Or, 

R — Sodium hydrate (deliquesced) , 

Calvert's crystal carbolic acid .... p. aeq. — M. (Huey.) 
The liquid formed is spoiled when it effloresces upon the sides of the bottle neck. 

The painfully caustic action of the sodium or potassium hydrate 
is modified by the carbolic acid. 

The application of Robinson's remedy is useful in the simpler 
cavities and about the undecayed but hypersensitive necks of teeth 
and on occlusal surfaces. It is escharotic to the gum. 

If this remedy or zinc chlorid be required about the periphery of 
deep cavities the plan suggested by Jack, of varnishing the cavity 
floor with chloro-percha as an impenetrable protective is valuable. 

A method similar to the use of Robinson's remedy consists in apply- 
ing carbolic acid to a cavity and then without removing it, placing a 
few granules of sodium dioxid. 1 Sodium dioxid alone in a slightly 
moist cavity, liberates nascent sodium hydrate (also H 2 2 ), which 
will destroy the gum protoplasm, and is somewhat effective in hyper- 
sensitive dentin. 

Carbolic acid in concentrated form may be applied to any cavity. 
Jenkins, of Dresden, has recommended that it be used hot; it is 
particularly useful for cavities containing masses of softened dentin. 
A variation consists in the application to the cavity, upon a pellet 
of cotton, and heating it with a hot burnisher. 

Sodium bicarbonate is at times an efficacious remedy, and may be 

1 H. J. Moore: Dental Review, 1906. 



HYPERSENSITIVITY OF DENTIN 



333 



freely applied to the moist cavity. A 20 per cent, solution of am- 
monium carbonate, applied for five minutes or longer, is useful. 1 

The nitrate of silver powerfully coagulates fibrillar protoplasm, 
forming the albuminate of silver, which turns black upon exposure 
to the light. It is useful in posterior teeth well out of view, and to 
which the rubber dam cannot well be applied. It is also useful 
about undecayed hypersensitive necks of molar teeth. It penetrates 
the dentin for a short distance. For this reason its use is ordin- 
arily confined to posterior teeth, though in some obstinate cases of 
hypersensitive necks of lower incisors and cuspids it may be used. 
To prevent the production of hypersensitivity in teeth ground for 
bridge-work, it should be applied over the entire crown. If amalgam 
be not present a bit may be rubbed over the silver nitrate to blacken 
the surface. Ready-made aluminum crowns set with temporary 
stopping may also be used for this purpose. It may be used in 
saturated aqueous solution upon the dried dentin, or the crystal 
rubbed upon the slightly moistened dentin. The crystal or fused 
silver nitrate rubbed upon abraded and sensitive occlusal surfaces 
often affords much comfort. 

Fig. 323 




Dentin treated with silver nitrate at a only; the entire surface subjected to acid 
action shows penetration at 6. (Miller.) 

Craven's method consists of taking up a few crystals upon a hot 
platinum wire, and then fusing them into a button upon its rough- 
ened end. This is then rubbed upon the dentin. 

Miller has shown that the silver deposit lessens the penetration of 
acid decalcification (Fig. 323). 

The subsequent use of sodium chlorid assists in partially removing 
the stains, argentic chlorid being formed. 



Thiesing: Dental Cosmos, Nov., 1903. 



334 DENTAL CARIES 

Register has suggested the use of iodin followed by ammonia for 
this purpose. 

Coming into contact with an amalgam filling, or a bit of amalgam, 
an intensely black deposit is instantly produced, which, while acid at 
first, is useful in slowly obtunding dentin in cavities out of view. 
Curiously enough, not all amalgams do this. It also occurs where 
amalgam fillings or alloyed gold has been in contact with dentin so 
there it is probably a reaction between silver- nitrate and copper or 
silver and not necessarily dependent upon mercury. 

For severe cases not yielding to local treatment at the time desired, 
the following has been recommended. 1 

1$ — Trioxymethylene 

Orthoform p. aeq. 

Make into a paste with carbolic acid. 

Or, 

1$ — Menthol crystals 5 parts. 

Phenol crystals 4 parts. 

Reduce to a syrupy liquid to be used in place of the carbolic acid in the above 

formula. 

This paste is applied to the cavity walls over even decayed 
dentin, covered with a pellet of cotton, and sealed in with temporary 
stopping or cement for twenty-four hours only. Formaldehyd gas 
is liberated in the nascent state and desensitizes the fibrils by harden- 
ing and fixing them as in histological specimens. The orthoform 
acts as an anesthetic during the action of formaldehyd. This prin- 
ciple has been used in cavities with the ordinary 37 per cent, 
formaldehyd solution, applied by the pressure method, and is useful 
about the hypersensitive necks of teeth. Buckley 2 has recently 
introduced a modification in a paste form having similar action. 

B- — Neothesin (Lilly) 3^o grain. 

Trioxymethelene 53 grain. 

Thymol 270 grain. 

Petroleum base, coloring matter, and fibre. 

(The figures indicate the approximate quantities in one application.) 
S. — Apply to dry dentin and cover with cement for twenty-four to forty- 
eight hours. 

In shallow labial cavities it is to be applied and covered with 
very adhesive cement. 

This preparation has excited argument as to its pulp-devitalizing 
power. Prinz claims that it is an agent penetrating and devitalizing 
the pulp, while many competent observers say that it does not do 
so even when intentionally used for that purpose. 

1 G. Mahe, M.D., Paris: Dental Cosmos, 1904. 

2 Items of Interest, December, 1914. 



HYPERSENSITIVITY OF DENTIN 335 

In shallow cavities and upon abraded surfaces, nitric and chromic 
acid accurately applied in small quantity upon a gold probe is 
useful. Any softened dentin must later be removed and filled. 

For very obstinate cases of cervical or occlusal hypersensitivity, 
Flagg recommended the use of the electric cautery, the spots to 
be seared. A very hot burnisher may occasionally serve. If this 
or silver nitrate will not serve filling cupped-out places must be 
resorted to. 

Aside from the treatment of hypersensitive dentin, at the time of 
operation, analgesics may be introduced for their power of gradu- 
ally lessening the hyperirritability of fibrillar protoplasm. If cotton 
wedges are introduced, antiseptic analgesics, particularly oil of 
cloves (or eugenol), equal parts of oil of cloves and carbolic acid, 
and phenol camphor, or Fletcher's carbolized resin, may be used on 
the cotton with advantage. Chloral and menthol, equal parts, 
made by rubbing in a mortar, etc., may be sealed in on cotton for 
a few days (Buckley). 

A partially prepared cavity may be moistened with eucalyptol 
and temporarily filled with temporary stopping or gutta-percha. 
This affords rest. If the gutta-percha leak, the cavity will be more 
sensitive. 

A temporary filling made by mixing zinc oxid with Fletcher's 
carbolized resin or eugenol to a stiff paste will endure for some 
time, and reduce hypersensitivity. It is also useful as an antiseptic 
sedative test filling. 

]$ — Carbolic acid, 

Colophony aa 5J 

Chloroform fgss — M. 

(Fletcher.) 

A temporary filling of zinc oxid and eugenol will set in the saliva 
and answer the purpose, a crystal of thymol may be added. 

In cavities not permitting exact excavation, oxyphosphate of 
copper cement left for a considerable time will often reduce exquisite 
sensitivity. 

The use of chalk applied nightly in a superficial cavity, as at the 
cervix, is useful for this purpose. 

In cases in which devitalization is intended, arsenic may be used 
as an obtundent to effect a deeper placing of another portion as a 
devitalizing agent; twenty-four to forty-eight hours are required for 
this purpose. If left long enough it will devitalize the pulp even 
through a large mass of dentin. 

There is no safety in short applications as a means of obtunding 
dentinal hypersensitivity. The pulp may die even after seeming 
excavation of all affected dentin. 



336 DENTAL CARIES 

Ninety per cent, of cavities may be comfortably excavated with 
sharp instruments by the aid of dryness and carbolic acid or simple 
obtundents. A small percentage require the use of strong caustics, 
etc., while in a still smaller number some of the extreme measures 
are necessary, though nitrous oxide and blocking are admissible in 
all cases if the careful operator prefers as most do not. 

During seasons in which acid fruits are consumed, much hyper- 
sensitivity may be induced. This should always lead to examination 
for cavities of decay, but such may not exist or may be properly filled. 

For hypersensitivity about undecayed necks of teeth, the mouth 
should be kept in an alkaline condition by means of dilute phenol 
sodique or sodium bicarbonate, or, better, by the use of more lasting 
mild alkalies, such as chalk, rubbed into the necks and interspaces, 
or milk of magnesia (the mouth rinsed with a small quantity and 
the excess expectorated the residuum left), or a combination of the 
two may be used. The manufacturers of milk of magnesia recom- 
mend a series of oil mixtures; 6 drops of any mixture to be shaken 
up with the contents of the original bottle as a flavor to remove 
the naturally raw taste of the preparation, which is disagreeable to 
some persons. 1 The following are two of the simplest: 

Ifc — Oil of bitter almond 1 part. 

Oil of anise 3 parts. 

Or, 

1$ — Oil of cinnamon 3 parts. 

Oil of wintergreen 4 parts. 

The use of potassium carbonate in glycerin is indicated and may 
be given to the patient for free use. The patient is directed to 
apply chalk thereafter. (See page 324.) 

For hypersensitive incisal edges or occlusal surfaces, Robinson's 
remedy may be thus dispensed with a caution as to its caustic nature. 

At times zinc chlorid, Robinson's remedy, and silver nitrate or the 
actual or electric cautery must be used by the operator. 

In a number of the localized cases fillings may be subsequently 
required unless rigid prophylaxis be practised. Prophylaxis may 
remove the superficial desensitized layer, and the application require 
renewal. I have been informed that a case of general hypersensiti- 
vity was cured by the lemon juice treatment given for systemic con- 
dition. The idea is worthy of attention. It might be explained 
upon the principle of induced alkalinity of salivary secretion as 
organic acids are known to increase the alkalinity of the urine. 

The use of potassium sulphocyanate internally in case of great 
general dental hypersensitivity has had good results claimed for it, 
especially in pregnant women. (See p. 271.) 

1 Items of Interest, 1905, p. 977. 



CHAPTER XI. 

DENTAL CARIES: THERAPEUTICS AND PROPHYLAXIS. 

According to the depth of invasion and variations in the thera- 
peutics involved, caries may be divided into eight stages, as follows: 

1. Superficial caries, or that stage in which the enamel has been 
partially decalcified, but the dentin not affected (Fig. 278). 

2. Simple caries, in which the dentin has been affected slightly, 
in such manner as ordinarily to compel the formation of a cavity 
and its filling (Fig. 284). 

3. Deep-seated caries, in which the complete excavation of the 
cavity renders pulp injury a possibility, but the pulp is not very 
dangerously approached (Figs. 281 and 291). 

4. Almost exposed pulp. This is a refinement of the preceding 
stage, in which pulp exposure becomes imminent during excavation 
of the cavity and special therapeutics are demanded (Fig. 324). 

5. Exposed pulp, in which the actual exposure of the pulp by 
decay or by accident or intention during excavation renders its 
treatment necessary, or in which disease of the pulp compels canal 
treatment. 

6. Perforation by caries, in which after pulp death secondary caries 
of dentin and cementum has caused an opening into the pericemental 
tract (an extension from the condition in Fig. 300). (See Fig. 325.) 

7. Loss of crown by caries. 

8. Loss of root by caries. 

Each of these stages of caries requires special consideration and a 
therapeutics adapted to each. 

THERAPEUTICS OF SUPERFICIAL CARIES. 

About cavity margins, beneath green stain, etc., along bucco- 
cervical margins, and at points of approximal contact of teeth may 
frequently be seen areas of enamel decalcification, the enamel not 
being entirely penetrated (Fig. 278). 

It is possible at times to remove the decalcified portion by means 
of carborundum strips, files, or disks. If the surface be highly 
polished by means of pumice and chalk, and subsequent prophyl- 
axis be employed, the practice may be endorsed for the better grades 
22 (337) 



r,3S DENTAL CARIES 

of teeth, and particularly in the anterior part of the mouth. As a 
rule, however, the attempt to remove supposed superficial enamel 
caries demonstrates the fact that the enamel is deeply affected, and 
in all probability the dentin as well. The attempt to remove such 
caries upon proximal surfaces by files and stones results in tooth 
deformity, the exposure of dentin to the fluids of the mouth, and the 
destruction of the contact points, except, perhaps, when in the 
anterior teeth a lingual approach is made. It is sometimes proper to 
remove the slight superficial caries found about a cavity, either prior 
to excavation in order to determine the real cavity boundary, or 
after excavation if such removal would give an even better tooth 
form, and lessen a recurrence of decay, or, in some cases, after filling 
when both filling and margin are reduced together to a proper 
form and integrity of enamel. Some judgment is required in such 
a matter, and no enamel should be so treated if any doubt exist as 
to its future integrity, but the cavity should rather be extended to 
include the doubtful area. (See Fig. 284 for contra-indieation.) 

It may be considered a safe rule to examine, by means of the electric 
mouth lamp, any cases of suspected superficial caries in order to 
determine the depth of enamel invasion. 

The large majority of such cases, especially in the poorer grades 
of teeth, will be found to be of the class called here simple caries. 

Upon the labial or buccal surfaces of anterior teeth a superficial 
decalcification may be found. Whether (1) this shall be removed 
and the surface polished, or (2) be left for the patient to care for 
by exact prophylaxis, or (3) be excavated and filled, depends upon 
the location, the depth of penetration, and the progress of the 
enamel decalcification. The writer has carried forward for a long 
time numerous white crescentic markings by prophylaxis which 
removes microbic plaques and food and aborts decalcification, 
though not removing the tissue decalcified. 

In posterior teeth staining with silver nitrate alone or by touching 
later with amalgam to produce a rapid deposit of silver, grinding 
off with stones and then touching with silver nitrate, or filling the 
actual cavity with oxyphosphate of copper and staining and watch- 
ing the remaining decalcification, have all given good results when 
conjoined with improved prophylaxis by the patient. Superficially 
decayed cementum may be removed or not and silver nitrate applied . 
This applies to only slight depths of decalcification. These spots 
are often deeper than at first thought and they should be somewhat 
forcibly penetrated with the explorer to determine the point; if 
fairly deep and in locations not readily cleansed they should be filled. 



THERAPEUTICS OF DEEP-SEATED CARIES 339 



THERAPEUTICS OF SIMPLE CARIES. 

The cases cited above as requiring excavation and all detectable 
cavities of very limited depth may be classed as cases of simple 
caries. The teeth should be wedged apart if this be needed for access, 
all decalcified enamel and dentin removed, the cavity properly 
extended and shaped, and, as a rule, a metal filling inserted. All 
fissures about a cavity should be freely opened to their extremities, 
and made a part of the general cavity. 

The extension upon approximal surfaces should include all super- 
ficial decay that cannot be so disked off as to bring the filling margin 
into the embrasures. 

The treatment of simple approximal cavities is a difficult question. 
Undoubtedly extension enhances the longevity of the fillings. At 
times, however, the cavities may be kept purely approximal and by 
the use of gutta-percha, silicate cement or combination of amalgam 
and zinc phosphate cement renewed or repaired as required, the case 
can be controlled for many years. This may be advisable in anterior 
teeth where gold may be objectionable or when systemic conditions 
or uncontrollable sensitivity warrant it. In the main, if endurable, 
cavities in posterior teeth should be extended, otherwise the renewal 
of the fillings will probably in time be necessary. In the anterior 
teeth esthetics often warrants keeping the cavities small. The 
question is one which can be settled after consideration of all the 
requirements. Subsequent prophylaxis is of importance, and to that 
end all fillings should be made as smooth and perfect as possible. 

If a simple cavity prove inordinately sensitive, the more powerful 
remedies may be freely used to reduce the hypersensitivity, and the 
cavity should be treated with carbolic acid before filling, particularly 
when gold is to be used in cervicolabial cavities of incisors. By this 
means the subsequent effect of thermal changes is lessened. 



THERAPEUTICS OF DEEP-SEATED CARIES. 

In this stage of caries there is usually, although by no means always, 
an easily discoverable cavity of size (Fig. 291). After the removal 
of ragged and overhanging enamel margins, and of loose debris in 
the cavity, it is noted that the response to thermal impulse is painful 
and prompt. In washing such cavities, water at a temperature of 
about 100° F. should always be used; cold or very hot water being 
only employed in cavity irrigation to test the promptitude of response 
upon the part of the pulp. It is better to do this habitually. 



340 DENTAL CARIES 

In treating hypersensitivity of dentin carbolic acid is to be pre- 
ferred, the mineral acids are avoided, and if strong agents like zinc 
chlorid or Robinson's remedy are used, the cavity floor is to be 
varnished with chloro-percha or "cavitine" varnish, which are 
impermeable. If necessary the sedative temporary methods may 
be employed or the various anesthetic methods may be used, pulp 
exposure being carefully avoided. (See p. 314.) 

The removal of all the softened dentin, which should be done in 
these cases, forms a cavity of such magnitude that proximity to the 
pulp is evident. The softening has proceeded for a distance beneath 
the enamel, so that when all softened dentin is cut away from beneath 
it the latter tissue may overhang the general cavity unsupported. 
These overhanging walls are cut away until the region of strong 
enamel is reached, and then it may be that the walls still overhang 
the general cavity. It is usually not necessary nor advisable to 
remove this portion of enamel. 

At the completion of excavation the pulpal wall of the cavity will 
be in fair proximity to the pulp. A blast of cool air from a chip 
syringe may produce an immediate response upon the part of the 
pulp, vigorous in proportion to the thinness of its dentinal covering 
and its irritability. 

In many cases non-conducting substances are required as inter- 
mediates between the pulpal wall and the metal filling. In many 
other cases the metal filling may be placed directly upon the dentin 
without danger. In some cases a simple layer of non-conducting 
varnish, such as "cavitine," 1 will be sufficient. In others zinc phos- 
phate or gutta-percha must be added. The degree of the response to 
a blast of cool air will afford a guide to the nature of the intermediate 
required if any be deemed necessary. In no case should varnish Or 
gutta-percha be allowed to remain in the portions of cavity that 
support the covering filling material, and which is subjected to the 
force of mastication. The resilient nature of such substances will 
cause the loosening of the filling and probably induce mechanical 
or infective irritation of the fibrils and through them of the pulp 
(Fig. 324). 

In some cases the undermined state of the enamel wall necessitates 
the use of an adhesive zinc phosphate as a means of support by 
replacing the lost dentin, and in such the pulpal wall may be covered 
and so protected from impact as well as from thermal changes. 



1 Cavitine is a solution of trinitrocellulose in subacetate of amyl. Gum sandarac in 
alcohol, gum copal in ether, or Canada balsam or gum dammar or colophony in chloro- 
form, about 30 grains or less to the ounce of solvent and a little hydronaphthol 
added, makes an antiseptic cavity varnish. 



THERAPEUTICS OF DEEP-SEATED CARIES 



341 



Fig. 324 




The action of zinc phosphate upon dentinal fibrils and the pulp 
being a matter of some doubt, it is better that the pulpal wall be 
varnished before it is introduced. The varnish not only acts as an 
impervious coating, but also serves as an additional non-conductor. 
If made antiseptic it is still more useful. 

After the cavity is prepared it is sterilized and dried, as described 
in the next stage of caries, is coated with varnish, and adhesive zinc 
phosphate plus 5 per cent, powdered thymol 
mixed stiff is packed into the undercuts and 
over the pulpal wall, and approximately formed. 

When set the enamel margins are freed of 
cement and the cement is excavated to the form 
required. In some cases cement can only be 
placed over the pulpal wall, owing to lack of room 
for both cement and the covering filling. In such 
cases the combined use of soft cement and gold, 
such as "moss-fiber" as a first portion or soft 
cement and amalgam, is useful. (See page 343.) 

In deep-seated caries the extension of cavity 
margins in such a manner as to prevent re- 
currence of decay is demanded. Upon approxi- 
mal surfaces the ideal conditions are an extension 
of buccal and lingual margins to a point which 
will permit a contoured metal filling to have 
its corresponding buccal and lingual margins 
well irrigated by the action of the tooth-brush 
and food in mastication. Often a slight alter- 
ation of tooth form, together with contouring 
of fillings, accomplishes the end desired without 
undue cutting of tooth structure. Thus the cervical margin may be 
slightly reduced with strips or disks to assume an absence of contact, 
but the enamel must not be totally removed. The lingual or buccal 
margin may be treated in a similar manner. 

The cervical margin of the cavity and filling are best protected 
when overlapped by healthy gum tissue, and if the gum be ap- 
proached, should be so arranged. The cervical margin should always 
be extended beyond the contact point in such cases, whether carried 
beneath the gum or not (see p. 259). Incisal margins are to have 
similar consideration. 

Firm approximal contact of fillings or filling and tooth are required 
to prevent packing of food into the interproximal space. This would 
both injure the gum and introduce the fermentable element in caries 
production. The point of contact should be neatly rounded to 



Diagram illustrat- 
ing the use of pulp 
protectors: V, a 

layer of varnish; GP, 
a layer of low heat 
gutta-percha, or in 
case of exposure a 
layer of Jodoformagen, 
or zinc oxid and thy- 
mol in which case the 
varnish is omitted ; 
ZP, zinc phosphate; 
with or without thy- 
mol added; M, metal 
covering. 



342 DENTAL CARIES 

produce a normal contact. This contact should be obtained even if 
the filling must be overcontoured. 

An exception may at times be made where a space has previously 
naturally existed, and the gum margin is healthy. 

Teeth should never be joined by fillings alone, as one or both will 
usually loosen. If necessary for the protection of the gum, both may 
be crowned and the crowns united by solder, or a staple may be 
placed in the pulp canals of the two teeth. About this a common 
filling may be built. It may be that gold inlays, locked in spacious 
"doll heads" on the occlusal surfaces of both teeth, and extending 
over to distal approximal surfaces as well as into the cavities, may be 
joined as a means of support. Pinlays may be used. The strain upon 
such fillings is very great when occlusion exists, as teeth are bodies 
with individual motion and are apt to be pushed away from the 
filling. (See Pyorrhea Alveolaris and Gingivitis.) 

THERAPEUTICS OF ALMOST EXPOSED PULP. 

In this stage of caries complaint is usually made that for some 
time pain has been produced by the presence in the mouth of cool 
or hot substances. Several classes of almost exposed pulps may be 
discovered after opening the cavity and removing the bulk of the 
decayed dentin. In the simplest class the pulpal wall may be found 
sound after removal of all decalcified dentin. This makes practically 
a case of deep-seated caries, and is to be treated as such, the close 
approach to the pulp simply demanding additional precautions as 
to non-conduction, prevention of compression, and infection. The 
cavity is to be neutralized with a solution of sodium bicarbonate and 
and dried; over the pulpal wall "cavitin" with hydronaphthol added 
or other antiseptic varnish, and dried again. 

IJ — Hydronaphthol gr. ij 

Alcohol gtt. xx — M. 

Add to the half-ounce bottle of "cavitine. " 

A thin wafer of softened gutta-percha is to be laid over the pulpal 
wall in such manner as not to interfere with the introduction of 
cement. In place of these any of the pulp capping cements may be 
used as a first layer (Fig. 324) . Adhesive zinc phosphate mixed to 
consistency just suited to the case may be pressed laterally into the 
undercuts, and will spread nicely over the gutta-percha without 
pressure. Under no circumstances must the superstructures depend 
upon the gutta-percha base as a support, as the filling may loosen 
or the wall be broken. (See page 340.) 

The operation may be varied for cases of but limited retaining 



THERAPEUTICS OF ALMOST EXPOSED PULP 343 

periphery by gently spreading the zinc phosphate over the varnish, 
or, in some cases, the gold and zinc phosphate or amalgam and zinc 
phosphate combination may be required. 

In the use of gold and zinc phosphate a portion of crystal gold is 
gently tapped into a mass of soft, quick-setting cement placed over 
the varnish and the setting of the cement awaited. The gold is then 
condensed and more added. 

With the amalgam and zinc phosphate combination, after placing 
the gutta-percha, varnish, etc., soft cement plus thymol is placed 
upon one cavity margin, and a ball of previously prepared amalgam 
is laid upon it. Pressure upon the amalgam by means of a ball bur- 
nisher causes the cement to be spread over the cavity wall in advance 
of the amalgam. It practically inlays the metal filling, but permits a 
better marginal joint with the metal. It has been called an amalgam 
inlay and deserves the appellation which, however, has been pre- 
empted by a previously devised but generally unused operation. 
The margins are freed of amalgam and cement, and the operation is 
completed with amalgam. It also prevents the shifting and dislodge- 
ment in any degree of the metal filling which sometimes occurs in 
the act of introduction, unless guarded against. 

This, of course, refers to locations in which the latter is indicated. 
The cement in the combination increases the adhesion and prevents 
leakage and the discoloration of the walls by the amalgam. A trifle 
of thymol added to the cement imparts to it an antiseptic character 
without impairing its integrity as a cement. 

The second class of almost exposed pulp is that in which thorough 
excavation would cause exposure of the pulp. 

If the dentin be of the disintegrated, boggy sort, it should be 
removed regardless of exposure; but if it be simply softened by 
decalcification and be quite firmly adherent to the cavity floor, and 
particuarly if it be somewhat thickly distributed, the deeper layers 
may be left in situ, as a pulp covering. 

In such cases all lateral walls should be thoroughly excavated and 
only a thin layer left over the pulp horns. While, without doubt, the 
tubules of decalcified dentin are liable to be invaded by bacteria, 
Miller has shown that frequently such dentin may exist without 
invasion. (See Fig. 294.) 

The argument that such dentin contains poisonous products of 
bacteria deleterious to the pulp does not seem borne out by results 
in carefully handled cases. Decalcification is not putrefaction. 

That some of these protected pulps may die is a fact not to be 
disputed, but that many live in security is also true. Whether such 
dentin can be recalcified has not yet been scientifically shown, but 



344 DENTAL CARIES 

certain cases treated with oxychlorid of zinc have shown evidences 
of it, and Miller records cases of hardening of such caries even 
without treatment. 

The decision (1) as to conservation of a pulp by this method, or 
(2) excavation to sound dentin or possible exposure and treating 
that by capping or devitalization rests with the particular practi- 
tioner who must decide upon the character of the dentin, possible 
pulp infection or the hyperemic or inflamed condition of the pulp 
according to the symptoms. I would suggest as favorable, cases 
with a good quality of simply decalcified dentin (or, of course, thin 
soundjientin) and without other symptoms than reasonable hyper- 
emia responding to therapeusis. The profession at large is beginning 
to turn to conservation as an avoidance of possible apical abscess due 
to^imperfect canal treatment. 

The treatment required for this dentin is: (1) Neutralization of 
the acid present; (2) saturation with a permanent antiseptic; (3) an 
antiseptic non-conductive covering. 

After drying, a weak solution of sodium bicarbonate or ammonium 
carbonate (diluted aromatic spirit) will accomplish the first require- 
ments. The dentin is then thoroughly dried and saturated with 
"cavitine" or other varnish containing hydronaphthol, or a solution 
of Canada balsam containing hydronaphthol, or thin chloro-percha 
containing aristol or iodoform, or the preparation known as "Jodo- 
formagen" may be spread over it, or oxychlorid of zinc, the fluid 
of which has been diluted one-third with water, may be used as a 
covering (use fluid, 2 drops; distilled water, 1 drop), or a mixture of 
zinc oxid and thymol may be melted over it. 

Williams 1 suggests that the decalcified dentin be first saturated 
with absolute alcohol for one minute, then dried, then wet with oil 
of cloves for one minute, then again dried, after which the varnish, 
etc., is to be used. Solution of sulphate of copper may be used to 
saturate the dentin, after which it should be dried and encased in 
varnish, etc. This last only in posterior teeth. 

The use of these preparations obviates the necessity of sealing 
temporary antiseptics in the cavity, as they are in themselves more 
or less permanently antiseptic. The rigid preparations are most 
convenient. Over them zinc phosphate, made antiseptic with 
thymol (1 to 20), is packed or flowed, if pressure be feared and if 
any doubt exist, the cavity is temporarily sealed with gutta-percha 
or temporary cement, usually a different color being employed. 
When all doubt is at rest the metal filling may be placed. In another 

1 Items of Interest, 1898. 



THERAPEUTICS OF ALMOST EXPOSED PULP 345 

method, useful in doubtful cases in determining the possible bad 
reaction of the pulp, a quite stiffly mixed paste of eugenol and 
Hubbuck's zinc oxid may be introduced into the base of the cavity, 
gently pressed to place with cotton, and covered with sandarac on 
cotton. At a subsequent sitting part of it may be left as a reason- 
ably firm antiseptic foundation. A trifle of thymol may be added. 
If desired, the entire cavity may be filled with it, or better, to a 
slightly concave surface. Exposed to the saliva it hardens to a 
degree sufficient to act as a cement temporary filling for weeks or 
months, or, occasionally, even years. 1 This method has a slight 
objection in that one is liable to remove all the material while exca- 
vating a part; so that the writer prefers in most cases to perma- 
nently apply Jodoformagen or its equivalent and then cover with 
good adhesive zinc phosphate plus thymol as a lining, then place 
gutta-percha base plate. The judgment proving correct upon test, 
the balance of the work proceeds after removal of the gutta-percha. 

In some cases of deep-seated caries in which gold filling is desirable, 
but in which linings are contra-indicated, yet in which immediate 
filling with metal would involve such thorough excavation as to 
endanger pulp vitality either as the result of excavation or subsequent 
thermal shocks, oxychlorid of zinc may be placed in the peripherally 
prepared cavities, and over considerable masses of decalcified dentin. 
If allowed to remain for several months (three to six) the oxychlorid 
stimulates the pulp to the formation of some secondary dentin, and 
complete excavation to a sound basis may be made. There is also 
some evidence of hardening of the dentin. This method is open to 
the possible objection that secondary dentin is a source of future 
trouble, but the method has its advantages in badly decayed anterior 
teeth. 2 In very deep cavities the fluid of the oxychlorid should be 
diluted one-third with distilled water for the first portion. 

In these cases porcelain inlays, with their underlying cement, 
should have due consideration as therapeutic means. 

In deep and very deep-seated caries, in situations in which dis- 
coloration is not of great moment jodoformagen may be placed 
over the pulpal wall, avoiding the bearings and the cavity filled with 
oxyphosphate of copper for its antiseptic value. The cavity may be 
entirely filled with it, or it may be used as a combination with 

1 Dr. S. Blair Luckie. 

2 In some cases of this sort seen by the writer, and observed for from ten to twenty 
years, the ill-results of oxychlorid of zinc claimed have not been observed. In one case, 
after sixteen years, a lateral incisor crown broke off, and the pulp was found to have 
receded, but was otherwise apparently healthy. The question is one of the advisability 
of immediate devitalization, with its advantages and disadvantages in anterior teeth, 
or of a possible remote pulp death, etc. 



346 btlNTAL CARlfiS 

amalgam. Copper amalgam alone ordinarily becomes disintegrated 
and caries recurs. Occasionally it lasts well (especially Sullivan's); 
copper and its salts are germicidal in a short time. The ordinarily 
good behavior of somewhat doubtful dentin under it is thus explained. 
To make the filling more lasting ordinary amalgam may be added 
to a lining of copper amalgam after the margins are freed or at 
least the copper amalgam feather edged. 

Dobrzyniecki 1 (Budapest), in eight experimental cases upon 
microscopically sound-looking dentin, claims to have found the 
Bacillus gangrense pulpse vital after months of enclosure under 
sealed dressings of camphor, concentrated carbolic acid, or eucalyp- 
tus oil. All other organisms were devitalized. As Arkovy's 2 experi- 
ments showed the decided influence of carbolic acid over this 
organism, and as root-canal antiseptics are nearly always successful 
in cases of moist gangrene of the pulp (Bacillus gangrenae pulpse 
Arkovy), the difficulty of destroying this germ by germicides left 
indefinitely in the cavity must be accepted with reservation. 

In some desperate cases with the walls frail, the cements, either 
zinc phosphate or so-called silicate cements, or oxyphosphate of 
copper cements, may be used as a last resort before crowning. The 
silicate cements are less soluble in the acids contained in saliva or 
formed from carbohydrates against the filling than are the zinc 
phosphates. 

Hinkins and Acree 3 claim that one-fifth of 1 per cent, is sufficient 
to dissolve the zinc phosphate, and that enough acid elements enter 
from the blood to affect it. 

The silicate cements dissolve more readily under friction than 
under the action of acid, so that of two fillings the one which is not 
exposed to attrition or brush action is usually in better condition 
after about two years. Much care is necessary to prevent the dis- 
coloration of silicate cements. 

These conservation methods apply only when it is considered 
proper to conserve a reasonably healthy pulp. Certain considera- 
tions of anchorage rendered necessary by weakness of walls also 
contra-indicate pulp conservation as does also evidence of profound 
pulp disease (which see). 

THERAPEUTICS OF EXPOSED PULP. 

The exposure of the pulp may be the direct result of caries; the 
removal of boggy, disintegrated dentin may produce it, or it may 

1 Soderberg upon Arkovy: Dental Cosmos, 1899. 2 Ibid. 

3 See Dental Cosmos, June, 1901, and March, 1905. 



THERAPEUTICS OF EXPOSED PULP 347 

be the result of the removal of a last layer of decalcified dentin 
or of the careless or inadvertent perforation of sound dentin by 
instruments. Fracture or abrasion are occasionally responsible for 
exposure. Erosion rarely causes it. 

Diagnosis. — After excavation of the cavity, washing with tepid 
water, and moderate drying, direct vision or a reflected image in the 
mouth mirror may reveal the area of exposure as a round opening 
occupied by a pinkish or red body. If the exposure be reasonably 
large, pulsation of the red body may sometimes be observed. The 
exposure may be so slight as to be invisible, the depth of the cavity, 
however, indicating that exposure probably exists. Bleeding is a 
certain guide, but bleeding from the gum margin must be borne in 
mind. Truman advises that finely carded cotton be gently passed 
over the cavity walls, exposure being detected by the momentary 
pain produced when the fibers pass over the area of exposure. 

As this test may fail, in cases of known exposure, it is not altogether 
reliable, but is fairly so when pain is produced, though hypersensitive 
dentin must be borne in mind. 

A finely pointed probe may be gently dragged over the pulpal 
wall and catches in the orifice of exposure, however small. A slight, 
quick start upon the part of the patient is usually elicited. This may 
consist simply of a winking of the eyelid. Flagg warned against 
requesting an affirmative nod by the patient, as this would cause 
injury to the pulp. Delicately used, this test is the most reliable in 
all classes of cases, and is not painful. 

It is to be remembered that disease may have caused a loss of a 
portion of a pulp horn, in which case the cotton test will fail; gentle 
exploration will detect the amount lost. Blood, or pus followed by 
blood, or sensation after entering the horn of the pulp cavity, are 
evidences of exposure. 

Excruciating pain following mastication, or pressure or suction 
exerted upon the cavity by means of the tongue, are subjective symp- 
toms indicating a probable diagnosis of exposure. Increase of pain, 
or throbbing pain following the use of salt, sweet, or acid foods, is 
fairly indicative of a practical exposure, but the indication must be 
confirmed by other tests. 

Treatment. — An exposed pulp is either to be capped or removed 
and the canals filled. 

The consensus of opinion is that ordinarily all pulps should be 
removed, except those freshly exposed by removal of simply decal- 
cified dentin and by accident and those in teeth with incomplete roots. 
There is no certainty that pulps exposed by caries or practically so 
will live under capping materials, but the attempt may be made 
at times for special reasons. 



348 DENTAL CARIES 

Freshly exposed pulps may be capped or removed. Perhaps a good 
rule would confine capping to anterior teeth of the better grades in 
patients in good physical condition, and to pulps in teeth having 
incomplete roots. At present all unnecessary pulp devitalization 
should be avoided in view of possible abscess. The advantages of 
capping are maintenance of tooth translucency and the avoidance 
of canal work. 

The disadvantages are: (1) Possible death' of the pulp by hyper- 
emia due to conduction of thermal changes. (2) An overproduction 
of secondary dentin, the production of pulp nodules, or other degen- 
erative changes, the pulp becoming exhausted and death ensuing. 
Increased difficulty of canal treatment may result. (3) Disease of 
the pulp due to infection beneath the capping material. (4) The 
time required for assurance of success or failure. 

The object sought in capping is the protection of the pulp from 
thermal changes, infection, and compression, as either is fatal to pulp 
vitality. This is best accomplished by placing in contact with the 
pulp an antiseptic paste beneath a metal cap, or an antiseptic 
cement having, when set, sufficient rigidity to permit other work 
to be done. In the latter case the capping material may be spread 
over the pulp by means of an instrument or be carried on oiled paper 
which may be stripped off after the cement has set. 

Prognosis is favorable for the cases selected as suggested. 

Pulp Capping. — The metal cap should be made of platinum or gold 
for anterior teeth. Tin, lead, copper or silver may be used poster- 
iorly. After punching or trimming to shape it should be made con- 
cavo-convex by pressing it into soft w T ood by means of the rounded 
end of an instrument handle. A film of wax is placed on the convex 
side; a warmed, small burnisher is attached, and the cap is adjusted 
in proper position by trying in the cavity. It is then to be filled with 
the capping material (a little of the latter placed in any depression 
at the point of exposure in order to exclude air) ; then one side of the 
cap is laid upon the dentin and the other gradually brought down, 
and the edges of the cap firmly adapted to the dentin. This causes 
the paste to exude from beneath the cap. Any excess is gently 
removed with an excavator if not of an immediately setting paste. 
A little soft, quick-setting, zinc phosphate cement plus thymol or 
oxychlorid of zinc cement is now run over the floor as a protection 
and when set more stiffly mixed zinc phosphate plus thymol is used 
as a lining and this covered with gutta-percha or temporary cement. 
This is then allowed to go as a test. Later a partial excavation 
of the cement is done or better zinc phosphate or silicate cement 



THERAPEUTICS OF EXPOSED PULP 349 

placed, or gutta-percha used as a further test, which is allowed to 
remain a year. 

These may be renewed as worn out if desirable, or a portion of 
the covering filling may be cut away and metal introduced to com- 
plete the operation. In all cases capping materials are not to be 
allowed to support the superjacent filling materials which should 
have their own support upon the cavity walls as shown in Fig. 
324. In case a plastic filling is desirable in any event, the opera- 
tion is to be completed at the time of capping or at a subsequent 
sitting. 

The materials used with success as pulp cappers are: 

1. A mixture of eugenol and zinc oxid (equal parts of carbolic 
acid and oil of cloves may be used as the menstruum). Hubbuck's 
zinc oxid or cement powder may be used. This is mixed to a con- 
sistency which will flow, yet set after some hours or days. 

2. Oxy sulphate of zinc, the fluid of which is a saturated solution 
of zinc sulphate in water. The powder is uncalcined zinc oxid. This 
will make a thin, creamy paste which flows readily and sets quickly. 
A trifle of aristol, iodoform, or hydronaphthol may be added to any 
setting cement. 

3. Plaster of Paris mixed with a 1 per cent, solution of formaldehyd 
in water will make an antiseptic, quick-setting paste. 

4. " Jodoformagen." This substance is said to have a mixture of 
eugenol and carbolic acid for the fluid, while the powder is of zinc 
oxid, containing paraform, the solid form of formaldehyd. It also 
contains salts of iodin. A cement is formed which sets quickly, 
and must, therefore, be made very thin when placed in the cap. 
This material has been successful as a capper even in exposures by 
caries, owing to its intense germicidal power. It is claimed that 
the formaldehyd penetrates the tissue of the pulp for a distance, 
yet permits its return to normality. 

5. Oxychlorid of zinc, with the fluid diluted with 50 per cent, of 
distilled water (1 to 2), will cap successfully. It is well to add a little 
powdered thymol to lessen irritation and add antisepsis. 

6. Crystallized thymol can be gently melted on the end of a 
burnisher and dropped on the point of exposure to crystallize, or 
a piece of a mixture of thymol and zinc oxid, made by melting the 
former and incorporating the latter, may be added to the drop of 
thymol in position and melted with a warm burnisher. Setting 
cappers may be used without metal. Of these capping materials 
the writer prefers jodoformagen, which though proprietary, has posi- 
tive sedative as well as germicidal and persistent antiseptic value. 



350 DENTAL CARIES 

Results of Capping. — If pain be initiated when the cap is placed 
and recur later, compression has occurred, and the capping must be 
removed, the pulp quieted, and the capping renewed or the pulp 
removed. Though no sensation be produced at the time of operation, 
a reaction to thermal changes may occur. If this gradually subside 
as counter-irritants are used, a diagnosis of arterial hyperemia (aseptic) 
is confirmed. If the reaction increase, the heat become more irri- 
tating than cold, and if at the same time paroxysms of pain or reflex 
pain occur, the diagnosis is that of venous hyperemia or infective 
.inflammation, according to the character of the symptoms, and the 
pulp must be removed. In cases of incomplete roots the large fora- 
men prevents the formation of a venous stasis. Even if the pulp be 
kept alive only until root completion, much good will be done. 

A pulp may remain quiescent for weeks or months and then un- 
favorable symptoms set in, or it may die without any apparent pain. 
It is probable that in the latter case some reflex pains have been felt, 
but not related with the tooth, in the mind of the patient. 

In the successful cases, either the orifice of exposure is covered 
over by a deposit of secondary dentin, or the pulp remains perfectly 
quiescent beneath the capping material, without formation of deposit. 

Even when a deposit occurs the pulp may die from the atrophy 
and degeneration attendant upon the formation of much secondary 
dentin, and when no deposit occurs infection following leakages 
about filling and capping materials may take place after years of 
apparent success. While capping may be, and has been, successful 
in all grades of exposure, there is no certainty of success in the 
exposure by caries. The tentative treatment necessary offsets the 
labor of canal treatment. The alternative to capping the pulp is 
its removal. This requires a special chapter (which see). 

THERAPEUTICS OF PERFORATION BY CARIES. 

The progress of secondary caries in the dentin about the pulp 
chamber hollows out the root until at least at one point the chamber 
wall is but a decalcified layer of cementum covered by decomposing 
dentin. At some point the pericemental tissue will be uncovered by 
excavation or by the carious process (Fig. 325). The crown will 
probably be badly decayed. Taking, as an example, a lower molar 
perforated at the bifurcation with the pericemental tissue hyper- 
trophied into the opening (fungous gum), its treatment may be 
described as follows : The gum is first to be pressed out with cotton 
medicated with an antiseptic solution or varnish. Fletcher's car- 
bolized resin, or aristol in chloroform, or sandarac varnish plus 



THERAPEUTICS OF PERFORATION BY CARIES 



351 



orthoform, will serve. The patient may assist by placing daily 
cotton pellets saturated with any of the mild aqueous antiseptics, 
pliers being furnished for the purpose. 

If immediate work be desired, polypoid fungous gum may be 
saturated with trichloracetic acid and cut away without much blood- 



Fig. 325 



Fig. 326 





Diagram of treatment of perforation 
by decay. 



Crowning of divided roots. (Evans.) 



letting by means of a large, sharp, spoon excavator, or novocain 
or ethyl chlorid may be used for local anesthesia or an electric cautery 
may be used. Large, rose-head burs are used to free the cavity of 
all decay. The canals are opened and treated. If further treat- 
ment be desired, or be impossible until the perforation is disposed 



Fig. 327 



Fig. 328 





Cantilever crown. The useless root 
should be extracted. (Evans. 1 ) 



Diagram of a lateral perforation treated with 
gutta-percha; successful for seven years, when 
breakage of the crown occurred including the 
perforation: GP, gutta-percha; OZ, oxychlorid 
of zinc; A, amalgam. 



of, metal or wooden pegs (the Downie broach reamers will serve) 
are placed in the canals and a reasonably thin layer of copper amal- 
gam is built about the pins and over the perforation. A slight 
movement of the pegs will permit their withdrawal, leaving open- 



Artificial Crown and Bridge-work. 



352 DENTAL CARIES 

ings in the amalgam through which the treatment may be subse- 
quently conducted. The amalgam is then allowed to harden (Fig. 
325). To carry on the treatment while hardening, formocresol on 
a cotton pellet may be inserted over the openings in the amalgam 
and sealed over with soft cement. 

After canal filling the canals may be further reamed for screws or 
pins, which are inserted and the operation completed with amalgam, 
or zinc phosphate and amalgam if the condition of the crown admit 
of it; or, if crowning be required, this is arranged for in the building 
up with amalgam. 

A long perforation at a bifurcation may practically divide molar 
roots. This is to be made a complete division after treatment of the 
canals. Each section may be fitted with a pin and amalgam stump, 
to which a gold barrel is fitted. The barrels are each given an occlu- 
sal face, or the two a common occlusal face, and soldered together 
(Fig. 326). 

If one root be unsuitable it may be extracted and the other used 
as a foundation for a cantilever crown, a spur from which rests 
slightly upon the occlusal face of the adjoining tooth (Fig. 327), or 
the crown may carry a spur which rests in an inlay or filling in the 
adjoining tooth. 

A smooth plaque of low-heat, white gutta-percha (not temporary 
stopping) makes an excellent covering for a perforation. It is made 
larger than the opening covered, warmed, pressed to place, and the 
edges sealed with a hot burnisher. The covering filling will retain 
it in position. The approach to the perforation should be widely 
funnelled to permit a ready adaptation. A splendid covering for 
accessible perforations is found in oxyphosphate of copper cement. 
The opening should be funnelled, the parts dried thoroughly and 
the cement properly mixed can be painted over the orifice, adhering 
tenaciously to the tooth and soft tissue without pressure. It exer- 
cises an antiseptic influence. If sepsis occur, the resulting abscess 
will occur opposite the perforation, or in some cases create a small 
pocket similar to a pyorrhea pocket. In all cases judgment must 
be exercised, and the attempt to conserve unsuitable cases avoided 
(Fig. 328). 

THERAPEUTICS OF LOSS OF CROWN BY CARIES. 

If the portion of crown left after excavation be self-sustaining, 
but incapable of retaining a filling in the cavity, pins or screws 
may be placed in the root canal or the pulp cavity may be enlarged 
and made retentive. A filling is then built about or into the anchor- 



THERAPEUTICS OF LOSS OF CROWN BY CARIES 353 

age so made. At times the remainder of a tooth crown will support 
a hollow metal crown. 

When the carious crown has broken away or filling has become 
practically impossible or undesirable, the original beauty or useful 
form of the tooth may be approximately restored by means of one of 
the many forms of dowelled porcelain crowns, specially constructed 
gold and porcelain crowns, or all-gold, hollow-metal crowns, or a 
broad band may be adjusted and filled in with amalgam after setting 
with cement, or where a portion of crown only remains soft amalgam 
may be used inside of the band to make the adaptation, and the band 
then filled in, completing the work on the side at which the band 
has no cervical adaptation. These operations have been successful 
for years, if the remnant of crown has any supporting ability. 

If an anterior root be so hollowed out by caries as to be incapable 
of supporting a dowelled crown, with or without a cast base, it may 
be extracted, and the operation of transplantation performed, or, 
later, an implantation may be made. 

In the former operation the existing alveolus is enlarged if necessary 
to accommodate a tooth; in the latter operation a new alveolus is 
created by means of appropriate trephines and bone reamers. The 
tooth is to be prepared as for replantation (which see). 1 

If teeth have been lost by extraction, the spaces created may be 
filled by means of bridge- work or plates of various sorts. 

By common consent crown and bridge-work is considered a 
special department of dentistry. 

Therapeutics of Loss of Roots by Caries. — This occurs in several ways : 

1. After loss of the crown and the extension of the carious process 
into the interior of the root. In the later stages this root is rendered 
valueless for crowning purposes, and should be extracted. In some 
cases a transplantation operation would be warrantable, as in case 
of a single incisor, the other teeth being relatively sound. (See above.) 

2. If an artificial crown has been so placed as to expose the joint 
to caries, the process may proceed to a considerable extent, but 
does not necessarily involve the root interior, owing to the presence 
of the pin. Filling with amalgam or other plastic, or the recrowning 
is demanded if feasible. The gum having grown in, much packing 
out may be required; ablation may be required as well. 

3. In some cases penetrating cervical caries will cause a partial or 
complete amputation of a lingual or buccal root of an upper molar, 
or, possibly, a bicuspid. The pulp, of course, will have died, at 
least at the carious area. 



1 For methods of implantation, see special chapter. 
23 




354 DENTAL CARIES 

The cavity of decay should be cleansed and undercut, and an 
occlusal tap made for free entrance to the canals. The canals are to 

be reamed with Kerr broaches. The canal 
Fig. 329 of the decayed root is to be enlarged with 

Kerr root reamers, after which everything 
is to be dried ; a canal probe, or the largest 
reamer used, which may have wax in the 
spaces between the blades, is passed through 
the tap across the cavity into the farther 
portion of the root canal. Good amalgam 
is to be thoroughly packed into the cervical 
cavity and hardened by wafering. When 
nearly set, the filling is supported against 
dislodgement and the canal probe is care- 
Method of restoring lost fully withdrawn. After appropriate steri- 

canal continuity. The cavity r -• £ 1 •-u i? r i .' 

should have more retention Nation of canals with formalin solutions, 
form than shown, a, amalgam, the canal is filled. If the decay has been 

severe, and fracture threatens, an iridio- 
platinum pin is to be fitted into the involved canal and the crown 
tap and the pin used as the canal former while filling the cavity 
and then withdrawn. Later after sterilization it is cemented into 
the canal, thus strengthening the root against a threatened fracture. 
If actually separated by decay, it is better to extract the separate 
root portion and trim the stump, as in ordinary root amputation. 
(See special chapter.) 

CARIES OF THE TEMPORARY TEETH. 

Caries of the temporary teeth differs but little from that of the 
permanent teeth. The pulp cavities are, however, relatively larger, 
and the intensity of the carious process often causes rapid exposure 
of the pulp. Owing to the flat character of the approximations of 
the teeth, there is often more approximal than occlusal caries, and 
the cavities often have weak peripheries. 

Children have a fear of dental offices, excited by unpleasant experi- 
ences or the talk of their elders, and they do not mention slight pain 
such as that excited by hypersensitive dentin. There is, however, 
abundant evidence that the dentin of the temporary teeth may be 
hypersensitive. In cavities of simple nature the fillings indicated 
for adults serve if the operations are well borne. 

The shapes of the teeth, the restlessness and fear of the little 
patients, and the free flow of saliva indicate, for the most part, the 
use of plastic fillings, though the rubber dam may often be readily 
used. In deep cavities not exposing the pulps, the methods employed 




CARIES OF THE TEMPORARY TEETH 355 

for adults, of varnishing or insulating with gutta-percha and the 
subsequent use of zinc phosphate as a lining under metal fillings, 
are indicated. (See p. 343.) Certain occlusal cavities having small 
orifices and large interiors are well, and often permanently, filled 
with pink gutta-percha. Zinc oxid and eugenol made into a stiff 
paste often fills cavities acceptably, and lasts as well as oxyphos- 
phate unless it is too freely masticated upon. 

If cavities are observed before pain has been complained of, and 
prompt and quickly subsiding response to applications of cold water 
is obtained, indicating a normal pulp, the cavity 
should be excavated, with more regard to re- FlG - 330 

moving the marginal caries than to thorough 
excavation, dried, and an application of a 20 
per cent, solution of silver nitrate made for a 
few minutes, the cavity being subsequently filled 
usually with zinc phosphate or copper cement. 

In cases of adjoining approximal cavities 
there is a disposition for the affected teeth to approximal cavities. 
press together and lessen the size of the dental 

arch. Bonwill advised as a practice, followed by uniformly good 
results in such cases, to cleanse the cavities (Fig. 330) and insert 
masses of pink gutta-percha base-plate. The constant biting upon 
the gutta-percha causes a separation of the teeth, which increases 
the size of the arch and affords additional space for permanent 
successors. Hollingsworth introduced the idea of placing a small 
piece or cap of metal at the cervix, bridging the interdental space. 
A bit of gutta-percha is to be placed on the under side of the cap 
to make a gutta-percha adaptation; then more is built over it. Bon- 
will advised that before the gutta-percha masses are inserted, small 
pieces of blotting paper saturated with carbolic acid be laid against 
the dentinal walls and the gutta-percha be packed over them. The 
more efficient and persistent antiseptic silver nitrate may be applied 
instead of the carbolic acid. Kirk advises that asbestos felt be 
heated to destroy any organic matter present in it which might 
combine with the silver, and then be soaked in a saturated solution 
of silver nitrate, dried, and kept in dark bottles away from the light. 
Small pieces of the prepared felt may be used as described. With 
cavities as good as shown in the illustration, wedging and contouring 
each tooth with amalgam, after the use of silver nitrate and varnish, 
is quite admissible after making suitable retention. There is no 
reason why occlusal extension for retention should not be made. 
The conditions will determine the choice of materials. 

The silver-nitrate method is particularly applicable to shallow 
cavities in which excavation for filling is impracticable. The dentin 



356 DENTAL CARIES 

surface is cleansed and dried, and the fused silver nitrate is rubbed 
upon the surface. This may be done after the method of Craven: 
a platinum wire is dipped into the powdered salt and held over a 
flame until the powder fuses into a button. By this means applica- 
tion can be directly and accurately made. The arch is apt to become 
somewhat contracted, and food is liable to wedge between the teeth. 
In most cases fillings should also be used. Combination fillings of 
zinc phosphate or oxyphosphate of copper and amalgam are of 
advantage in case of frail walls. For the anterior teeth silicate, 
zinc phosphate, and gutta-percha fillings are useful, and for the 
posterior ones Ames' oxyphosphate of copper serves a good purpose. 

Fig. 331 




Right upper temporary molar disked lingually and filled. 

Caries is very liable to occur upon the approximal surfaces of the 
second temporary and first permanent molar. If the former be 
found largely decayed distally, the latter will usually be found decayed 
on the mesial surface. Amalgam in cavities well extended buccally 
and lingually, or gutta-percha, serves well until the second temporary 
molar is lost, when a good gold filling may often be introduced 
before the second bicuspid erupts. 

Well-contoured fillings must be inserted in such a case. As a 
preventive measure during eruption of the first molar, the second 
temporary molar may be disked to the form shown in Fig. 331. 

If incipient or simple decay has occurred on the two teeth, or 
even the second molar alone, it is then best to wedge the teeth apart 
and to make a disk separation (on the temporary tooth only) from 



RECURRENCE OF CARIES 357 

the lingual or buccal side, or both, and to contour the filling even in 
exaggeration, so that a minimum of contact shall exist. Any sur- 
face of dentin exposed by the disking should be included in the cavity, 
or, if this be not possible, then it should be rubbed with silver nitrate. 

Such surfaces should be carefully observed at regular intervals; 
indeed, if prophylaxis can be regularly instituted early and before 
caries of the first permanent molar, much good will be done. 

The pulp diseases resulting from caries of the temporary teeth will 
be considered with those of the permanent teeth. If the temporary 
teeth be so badly decayed as to be hopeless, so far as filling is con- 
cerned, they should be extracted. Occasionally the encircling of the 
teeth with pure gold bands cemented to place, or filled in with amal- 
gam is good practice. 

In the main the temporary teeth, especially the molars, should be 
filled with some view to the longevity of the fillings, as they often 
have to do service for years; malocclusion of the permanent teeth 
may be prevented, and the general health of the mouth is improved. 

The child should always be treated with kindness and truthfulness 
to establish faith, yet with sufficient firmness to command control. 

Under no circumstances should the child be given an excessive 
dread of dental operations, or be broken by nervous shock, as this 
attitude defeats the object sought. 

In one extreme case in which the child had never endured dental 
work, chloroform followed by ether was given and fifteen plastic 
fillings inserted. N 2 and might be used for the purpose. 



RECURRENCE OF CARIES. 

Passing over, as disproved by Miller, the theory of Palmer, that 
caries recurs about fillings as the result of electric action (see p. 242), 
it may be stated, as proved by scientific and clinical experience, that 
it recurs because after teeth have been filled, conditions exist which 
may favor the collection of microbic plaques and stagnant food 
material even more strongly than the original conditions, and that 
when recurrence has been prevented, the work has been done in such 
a manner as to prevent such collections. The specific defects which 
favor the formation of bacterial plaques may be epitomized as follows : 

1. Lack of approximal contact (food wedging between teeth). 

2. Roughness of the filling at an otherwise good approximal contact 
point which menaces the approximating tooth or the margin of the 
cavity by causing food retention and the spreading of microbic plaques. 

3. Unremoved excess of filling material at margins producing a 
ledge which collects food, etc. The edge of a crown may act in a 



358 DENTAL CARIES 

similar manner. An excess well beneath the gum is more apt to 
produce gingivitis than caries. 

4. Exposure of the cavity margin due to lack of covering by the 
filling material, whether not properly placed, flaked away, or due to 
fracture of margin during the filling process or subsequently thereto. 

5. Exposure of the cavity margin due to shrinkage or shifting of 
the filling material. The use of material not enduring mastication 
in places subject to it; the washing out of cement from the joint 
of an inlay or combination filling or dowelled bandless crown has 
much the same effect, though often much delayed. 

6. Solubility of the filling material, permitting the cavity wall to 
become exposed. 

7. Roughness of tooth surface, produced by polishing fillings with 
rough approximal trimmers, coarse grit strips, disks, or wheels. 
Exposure of dentin by overpolishing may be classed with the above. 

8. Lack of hygiene of surfaces which tend to decay, partly due 
to lack of extension of cavity margins. Even poor margins, if well 
extended, may not decay, whereas existing at or near contacts they 
are menaces. Lack of extension of approximal cavities often causes 
failure, through failure to include all carious enamel. Lack of exten- 
sion of a filling into a fissure adjoining it, which fissure may be 
decayed or invite subsequent decay. Lack of extension of labial 
cavities sufficiently under the gum cervically and in the mesial and 
distal direction, leaves a tissue vulnerable to microbic plaques if not 
already attacked superficially. 

Treatment. — The treatment of recurrent caries does not differ 
materially from that of primary caries. 

Repairs to obliterate crevices, breaks, or new decays may often 
be made if seen early, but so often is it the case that apparently 
slight recurrences are found after removal of the filling, to involve 
the entire cavity wall, that the only sound recommendation applic- 
able to all cases is that the filling be removed and the cavity repre- 
pared and refilled. The exception exists when, after the new cavity 
of decay is all excavated, the adaptation of the filling is seen to be 
perfect. Decay at two or more points of recurrence not subject 
to accurate repair, or general inferiority of the filling should condemn 
the entire piece of work. 

PROPHYLAXIS OF CARIES. 

The prophylaxis of caries involves the removal of its causes at 
frequent intervals. The condition under which this is applicable 
and the prophylactic treatment is fully considered in the special 
chapter on prophylaxis. 



SECTION VI. 

DISEASES OF THE DENTAL PULP. 



CHAPTER XII. 
CONSTRUCTIVE DISEASES. 

Diseases of the dental pulp are both acute and chronic. Accord- 
ing to the anatomical features, they may also be divided into con- 
structive and destructive. The acute diseases are usually destruc- 
tive; in the chronic, structural and constructive changes are com- 
monly noted. 

Pathologically there is no abrupt line of demarcation between 
diseases of the dentin and those of the pulp, as the dentinal tubules 
contain the fibrillar prolongations of the odontoblasts of the pulp. 
Effects produced upon the fibrils cause, therefore, a pulp reaction 
which may lead either to a constructive or destructive activity 
according to the grade of hyperemia or inflammation set up. The 
pulp diseases likewise cannot be sharply defined, as they are to some 
degree interdependent. For example, mild hyperemia may cause 
pulp nodule formation while the presence of the latter may induce 
more severe hyperemia or inflammation. 

CONSTRUCTIVE DISEASES OF THE DENTAL PULP. 

The constructive diseases of the dental pulp include all the sec- 
ondary dentin formations, tubular calcification, the formation of pulp 
nodules and calcareous degeneration of the pulp. 

Tubular Calcification. — Definition. — By tubular calcification, or, 
to express the condition more accurately, tubular dentinification, is 
meant the change that occurs in the dentin which leads to an obliter- 
ation of the dentinal tubuli by deposition of dentinal material along 
the inside of the walls of the tubules, with a corresponding atrophy 
of the fibrils. It is a sclerosis of dentin analogous to osteosclerosis. 

Causes and Occurrence. — The apparent cause is a mild degree of 
irritation, not passing the stage inducing construction or deposition 

(359) 



360 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

(increased function) and apparently caused by direct irritation of the 
fibrils, more particularly through the action of thermal shock, brush- 
ing, mastication, or action of acids. It occurs in the course of mechan- 
ical abrasion and erosion of the teeth, under metallic fillings, and 
probably a modification of the process precedes the slow invasion of 
dental caries forming the so-called transparent zone (see page 290). 
It begins at once the enamel is removed from the dentin at any point, 
and the dentin subjected to irritation, showing it to be due to a 
stimulation of the whole odontoblastic cell (including its fibrillar 
prolongation) . It occurs in some degree as a normal vital change due 
to age. It also occurs in pyorrhetic teeth as a result of pulp stimula- 
tion, and is the probable explanation of the dense polished look of 
dentin often seen upon removal of fillings (Figs. 240, 291, c, and 301). 

Pathology. — The fibril is lessened in diameter as the lumen of the 
tubule becomes smaller. There is sometimes an increased, but more 
often a lessened, sensitivity of the dentin. 

Other phases of the condition are discussed under transparency of 
the dentin, to which the disease corresponds. (See p. 290.) 

The altered dentin becomes translucent, acquiring a horn-like 
appearance, and, usually, secondary dentin formation begins coinci- 
dently with it. Andrews claims that granules of calcific matter are 
pushed into the fibrillar by the odontoblasts and deposited along the 
inner wall of the tubule, even to obliteration of them. These gran- 
ules give the color to abraded dentin in the region of the pulp cavity. 

Hanazawa 1 recently has shown that there is a slight interstice 
between the fibril and tubule wall in which liquid circulates. He 
also has shown numerous branches from the fibrils penetrating into 
smaller branching tubules. This affords anatomical basis for Andrews' 
view by which we understand calcific matter to mean calcoglobulin 
or soft dentinal substance which may be regarded in the light of a 
dentinal plasma, composed of lime and albumen and capable of con- 
solidating tubules or even of filling slight inequalities under fillings. 

Tubular calcification is, for the most part, to be regarded in the 
light of an effect due to a physiological process. It may be regarded as 
a physiological barrier erected against the progress of caries, erosion, 
or abrasion, threatening the invasion of the pulp. While it delays 
the disintegration of the tissue, it does not prevent it, because of the 
overwhelming character of the cause, but if the cause be removed it 
consolidates the surface as in eburnation (q. v.) In the cases due to 
age or the irritation produced by leucomain retention, it is probably 
a local expression of a general sclerotic change, the intercellular 

1 Dental Cosmos, February and March, 1907. 



SECONDARY DENTIN 



361 



substance (tubule wall) being formed at the expense of the cellular 
(fibrilla). In senility the change in the dentin may cause the teeth 
to be almost transparent. It requires no treatment. 



Fig. 332 



Fig. 334 




Secondary dentin 
formed after exposure 
of pulp by fracture 
during extraction. 

(Tomes.) 

Fig. 333 




Bicuspid in which a 
formation of second- 
ary dentin has failed 
to obviate perforation 
of the pulp cavity by 
resorption. (Tomes.) 




Harding's case of united fracture. The uniting material 
is of coarse osseous structure with numerous lacunal spaces. 
(Tomes.) 



Secondary Dentin. — Definition. — By sec- FlG - 335 

ondary dentin- is meant a deposit of dentin 
upon the wall of the pulp chamber, as the 
result of pulp stimulation after the pulp has 
enjoyed a physiological period of rest from 
dentin formation. It is always attached to 
the dentin. It is generally an accompaniment 
of tubular calcification. (See Figs. 240, 291-c, 
and 301.) 

Causes. — The cause of formation of secondary 
dentin is a stimulation of the pulp to increased 
functional activity. This stimulus may be pro- 
vided by any constant irritation of the dentinal 

fibrils, as, for example, when exposed at necks of teeth, upon abraded or 
eroded surfaces, or within cavities of decay. The presence of metallic 




Elastic layer of 
calcific material formed 
over an exposed pulp. 
(From a case.) 



362 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

fillings, conductive of thermal changes, may provide the necessary 
stimulus. Gold crowns upon ground-down crowns of vital teeth have 
a similar effect; the underlying cement may be irritating enough. 
The slightly irritative effects of oxychlorid of zinc used as a pulp 
capping or as a cavity lining often produce much secondary dentin. 
A pulp capping may provide the stimulus and new dentin fill the 
orifice of exposure. Absolute exposure without treatment has been 
recorded as productive of secondary dentin. In two cases described 



Fig. 336 



Fig. 337 




Fig. 336. — Secondary dentin filling the pulp chamber is a case of abrasion of a 
cuspid tooth: a, portion lost by abrasion; c, abraded surface; d, secondary dentin, 
filling a portion of the pulp chamber, and acting as a protection to the pulp; e, slender 
point of the pulp — irregular deposits are seen on the walls of the pulp chamber, as at 
/; g, cylindrical calcifications in the root portion of the pulp chamber. 

Fig. 337. — Secondary dentin from the same specimen as Fig. 336, magnified suffi- 
ciently to show the difference in primary and secondary tissue: a, abraded surface 
crown; b, secondary dentin; c, primary dentin; d, junction of primary with secondary 
dentin; e, remains of pulp tissue; /, small oval masses of calcific material. (Black.) 



by Charles Tomes, pulps widely exposed by fracture of crowns during 
extraction covered themselves completely in. The histological record, 
as seen in the photomicrograph, demonstrated that a plastic exudate 
was first exuded (plasma as previously defined above), which later 
calcified as an amorphous mass. 

Xext an irregular lamina was formed, and lastly, dentin containing 
tubules. It is to be inferred that both the pulp cells and the odonto- 
blasts may take part in the process (Fig. 332). 



SECONDARY DENTIN 



363 



I have seen one case in which a wide exposure had been covered in 
sufficiently to enable me to gently indent the covering,, which was 
convex, with a ball burnisher. Upon removal of the instrument it 
resumed its original shape, owing to its elasticity. The periphery of 
the original exposure was clearly defined (Fig. 335). In another case 
of known exposure with bleeding the patient kept eugenol on cotton 
in the cavity. After several weeks the exposure could not be again 





ilPL ' : "i! fBi 




Dentinal tumor within pulp chamber: A, diagram of the tooth, with dotted line 
showing the position of the section B. In B the pulp chamber is shown in section, 
nearly natural size, showing the tumor within. C is an illustration of the tissue of the 
tumor; a, a, the primary dentin; b, irregular tubules connecting the newgrowth with 
the primary dentin — most of these are very dark and irregular; c, c, a calcospherite 
included in the mass; d, apparently a bloodvessel calcified; e, calcified tissue; /, a 
finely granular mass; g, a spur of very transparent dentin. Dentinal tubules appear 
at h, h. (Black.) , 

discovered. Age seems to be a cause of general secondary dentin 
formation, but no doubt certain forms of irritation are introduced 
competent to produce the changes; for example, slight looseness of 
teeth, causing a constant pulp stimulation. At times reflex irrita- 
tion seems to be a competent cause, as in cases of partial abrasion 
the unworn teeth may be affected in equal degree with the worn 
ones. (Black.) For theory see pages 381 and 385. 
It is also true that any form of chronic irritation of the pericemen- 



364 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

turn of a tooth may produce arterial hyperemia of a pulp which will 
lead to the formation of secondary dentin or pulp nodule or both. 
Non-occlusion, mal-occlusion, pyorrhea alveolaris are typical ex- 
amples of the non-septic and septic classes of irritation. 

Pathology and Morbid Anatomy.— The formation is usually noted 
opposite to some area of injury, and may be distinguished from 
normal dentin by its translucency, or sometimes by its color, which 
may be a light brown. The deposit may be of fairly regular or 
irregular distribution, and even tumors attached to the dentin have 
been described (Fig. 338). 



Fig. 339 



Fig. 340 





Fig. 339. — Illustration of the narrowing of the pulp chamber in a molar (superior) 
by the deposit of secondary dentin resulting from abrasion, showing the portions of the 
chamber in which the deposit usually occurs. The light-shaded portion (b) shows the 
original dimensions of the chamber, which, in this instance, seems to have been pretty 
large; a, a point of deep abrasion; c, c, remaining pulp chamber, which is mostly 
filled with irregular masses; d, one of the root canals. It will be observed that the 
narrowing of the root canal is within the original pulp chamber. (Black.) 

Fig. 340. — P.D., primary dentin; S.D., secondary dentin; P, pulp chamber; D, D, 
nodules. 

Black has shown that in the deposits against normal dentin the 
first-formed portion contains an almost normal number of tubules, 
but their direction is sharply changed. As the deposits become 
thicker the tubules become fewer, and finally the dentin becomes 
amorphous in character (Fig. 341.) 

Black relates these appearances with the gradual atrophy and dis- 
appearance of the odontoblasts. As the pulp becomes smaller it 
also necessarily undergoes atrophy. 

Hopewell-Smith, 1 treating of secondary dentin under the title of 
" Adventitious Dentin," mentions several varieties: (1) Fibrillar, or 
that containing tube-like markings finer and less regular than in 
normal dentin. This would correspond to that in Fig. 338, h. (2) 



Histology and Patho-Histology of the Teeth. 



SECONDARY DENTIN 365 

Areolar, that containing interglobular spaces formed by the non- 
union of calcospherites. (3) Cellular, in which the cells of the 
pulp remain encapsulated in the calcifying matrix. (Fig. 342.) 

(4) Laminar, in which laminated spherites appear (Fig. 338, c). 

(5) Hyalin, having a granular or ground-glass-like appearance (the 
amorphous substance of Black) (Fig. 338,/). He regards the adven- 
titious dentin as formed by pulp cells rather than by the odontoblasts. 
In these cases the pulp deposits calcoglobulin against the dentin. 

Apparently in some of Black's cases the calcoglobulin was deposited 
about preexisting fibrillar which continued to persist in the new 
formation, the remaining odontoblasts receding, while in Tomes' 
cases the pulps were compelled to calcify a plastic exudate as a sort 
of basis for the beginning of tubule formation. This is probably the 
case in formation of secondary dentin as a repair of exposure under 
a cap. Black has shown that in abrasion the deposit is more regular 
than in caries, without doubt due to the fact that the thermal irrita- 
tion in caries is more irregular than the irritation of the fibrillar by 
abrasion. A deposit projecting irregularly from any point about the 
pulp cavity side into the pulp is called a " dentinal tumor" (Fig. 338). 

The entire crown may be removed by abrasion and in rare cases 
even by caries, and yet the pulp be protected. In some cases the 
protective action ceases and the pulp becomes closely approached 
or exposed (Fig. 214), probably due to a cessation of secondary dentin 
formation, the result of degeneration and loss of odontoblasts, or it 
may be due to very rapid wear (a later stage of Fig. 337). 

The mode of deposition upon the sides of the canal in abrasion, 
shown by Fig. 336, is quite characteristic, and sometimes annoying 
in that it permits an unlooked-for exposure, which, upon cocain 
anesthesia, causes one to follow a fine opening for an eighth of an 
inch or more before finding a proper canal. 

Deposits in canals may occur, lessening their lumen and increasing 
the difficulty of canal exploration (Fig. 340). 

"Secondary growths in cases of abrasion are not confined alone to 
the abraded teeth, but other teeth which have escaped wear may be 
affected in equal degree. In all of these cases there is direct evidence 
that the odontoblastic layer has been stimulated to increased 
activity and produced the regular secondary deposition." 1 (See 
Reflex Hyperemia of the Pulp, p. 385.) 

In case of advanced occlusal abrasion the area representing the 
cross-section of the original pulp cavity sometimes contains secondary 
dentin so transparent that one seems to look into the pulp cavity, 

1 Black: American System of Dentistry, vol. i. 



366 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

while in the same individual other similarly abraded teeth may have 
the more characteristic opaque deposit which may even be of brown- 
ish color. 

Secondary dentin is very often accompanied by other constructive 
changes in the pulp — i. e., pulp nodules and calcareous degeneration 
(Figs. 340 and 346). 

Miller has shown that dentin resorption by the pulp may be 
repaired by a new deposit of secondary dentin, which Hopewell- 
Smith has shown to be of the nature of cementum (osteodentin). 
(Fig. 364.) 

Fig. 341 




Calcification or deposit of secondary dentin, resulting from caries of an incisor: 
A, diagram of section of incisor, showing caries at a, and secondary dentin at b. B, 
illustration magnified 200 diameters, to show the tissue of the secondary dentin: a, 
pulp chamber; b, b, secondary dentin; c, primary dentin. It will be noticed that the 
dentinal tubes in the secondary dentin gradually disappear, giving place to a clear 
calcification. (Black.) 



Tomes 1 describes and illustrates a peculiar case of united fracture 
occurring in the practice of Mr. Harding. In an incisor an oblique 
fracture occurred which entirely separated the fractured segment, 
yet a plastic exudate occurred which, when calcified, attached it to 
the fixed portion of the tooth. The new formation did not resemble 
dentin in structure (Fig. 334). 

Fig. 243 illustrates a case «of repair of an incisor fractured at a 



1 Dental Surgery. 



SECONDARY DENTIN 



367 



point well up beneath the gum, a condition reasonably insuring 
asepsis. A firm reattachment occurred. Fig. 241 shows the soft 
tissues engaged in such a repair. I have seen such a fracture which 
resulted in pulp death and the coronal portion remained in situ for 
two years (according to the patient). This would give time for such 
a plastic exudate to form. In another case I was compelled to 
remove a pulp for hyperemia two months after a fall fractured a 
tooth in this location. This and Fig. 241 shows that under aseptic 
conditions the pulp may live and at least assist in forming the 
attachment. 

Fig. 342 




Osteodentin: A, outline of incisor, showing a narrowing of the root canal at b by 
a deposit of osteodentin. B, illustration of the tissue: a, primary dentin; b, line of the 
beginning of a growth of secondary dentin; c, secondary dentin; d, layer of granular 
matter; e, osteodentin; this has the lacunae at g and dentinal tubes at k; f seems to be 
the surface of the osseous deposit ; i, irregular crystalline deposits ; h, the pulp chamber. 
X 350. (Black.) (Tomes.) 



Kirk 1 records a case of immediate replantation in early life, followed 
in old age by root resorption. The tooth, when extracted, contained 
secondary dentin, which could only have formed as the result of a 
reattachment of the pulp. 

W. H. Trueman 2 reported that hypersensitive dentin was noted 
some years after a replantation under similar conditions. 

Osteodentin. — Tomes states that secondary dentinal deposits may 
assume the character of osteodentin, a form of dentin found in the 
teeth of some animals, in which the tissue presents combined char- 
acteristics of both bone and dentin. He cites the example also that 
elephants' tusks are frequently repaired with osteodentin after injury. 



Proceedings of the Academy of Stomatology, 1902. 



2 Ibid, 



368 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

The specimen illustrated (Fig. 342) was taken from a human case in 
which the coronal portion of the pulp chamber was almost obliterated 
by a deposit of secondary dentin. Probably some of the pulp cells 
have taken on the characteristics of osteoblasts. Tissue resembling 
cementum seems to be frequently found as a tissue of repair. 

Results of Secondary Dentin. — The formation of large masses of 
secondary dentin unquestionably brings about a degenerative con- 
dition of the pulp which may become a cause of neuralgia. The con- 
struction may itself be the cause or pulp nodules may be associated 
as another expression of construction due to the hyperemia induced. 
The pulp may die through atrophy and degeneration, and, becoming 
infected, may produce pericemental irritation. In one case seen the 
secondary deposit in the pulp chamber had separated the canal fila- 
ments of the pulp of a multirooted tooth into independent pulps, 
one of which was dead and the others alive and undergoing degenera- 
tion. The specific symptoms were those of pericementitis — i. e., 
elongation and tenderness to percussion. 

In another case of a first upper bicuspid the lingual filament was 
perfectly covered in and vital. The buccal filament, likewise enclosed 
and isolated, contained an abscess within the pulp. 

The symptoms complained of, however, were those of acute peri- 
cemental irritation, simulating incipient apical abscess (Fig. 371). 

In Burchard's case a molar containing a deep cavity filled with 
zinc phosphate gave vague pain, finally referred to the tooth, which 
responded only faintly to hot applications and not at all to cold ones. 
Secondary dentin was found complicated by calcareous degeneration 
— i. e., a degenerated pulp was present. Fig. 340 will illustrate. 

It has been shown by Hopewell-Smith that microorganisms may 
enter the pulp by way of the spaces or tubes in adventitious dentin. 

In certain cases a deposit extends well into a canal, totally obliter- 
ating it for much of its length. Unless symptoms be present it may 
ordinarily be left. In such cases thermal tests for pulp vitality seem 
often inconclusive. The electric current should be a more satisfac- 
tory means of diagnosis, provided the dentin be moist. It may fail, 
however, even though the pulp is vital. Radiography may show the 
condition in the cases of the larger root canals. Secondary dentin is 
sometimes quite hypersensitive, as shown by attempts at entering 
the pulp; in most cases it is quite insensitive until the pulp is reached. 
For this reason in attempted high-pressure anesthesia in such cases 
one may often drill almost to the pulp or to it without the anesthetic. 
The pulp is degenerate in such cases. This does not mean that sub- 
sequent disposal of the pulp will be easy. It is also difficult, as a rule, 
to force cocain through secondary dentin, even with a compound 



PULP NODULES 369 

syringe, and arsenic acts slowly, though it devitalizes if the dentin 
be sensitive. (See Dry Gangrene.) 

Treatment. — Secondary dentin which has been regularly deposited, 
and particularly in the canals of anterior teeth, calls for no treatment. 
Should, however, great hypersensitivity of the dentin and pulp, or 
pulp disease, be evident or inferred from symptoms, the pulp should 
be removed. Canal opening may involve a search of some difficulty 
and necessitate the removal of much dentin. The canals may be 
much constricted, especially at that portion nearest the pulp cham- 
ber. As a rule penetration of this is usually rewarded by the finding 
of operable canals. The condition may be more or less complicated 
by the presence of pulp nodules or calcific degenerations in addition 
to the secondary dentin. 

Pulp Nodules. — Definition. — Pulp nodules (pulp stones, nodular 
calcifications) are masses of more or less translucent, calcific material, 
apparently the result of secretion, having a fairly definite histological 
structure differing from that of dentin, and occupying a position 
within the pulp substance and not as a rule attached to the dentin. 
Rarely they are fused with the dentinal walls of the pulp chamber, 
and then are included by formation of secondary dentin about them. 

Causes. — While these growths may occupy the pulp chambers of 
teeth in which the pulp has been the seat of direct irritation, their 
occurrence is by no means confined to such teeth. They are found not 
only in teeth which have suffered abrasion, erosin, and slowly pro- 
gressing caries, but, as pointed out by Black, they may, and frequently 
do, form in other teeth of the same denture which are not directly 
involved in the irritation. This investigator notes that irritation of 
the pulp of one tooth of a denture very frequently causes a general 
hyperesthesia (due to mild reflex hyperemia) of the pulps of all of 
the teeth. Pyorrhea producing tooth movement or apical peri- 
cemental irritation can produce arterial hyperemia of the pulp and 
thereby pulp nodules. This is due to the constructive effect of mild 
arterial hyperemia which so far as is known is the probable proximate 
cause of all constructions. Even when inflammation is present there 
is always a zone of arterial hyperemia. (See pages 381 and 385.) 

Secondary dentin and nodules or pulp hyperemia may occur in 
sound teeth ground for crowns. This simply indicates a necessity 
for antisepsis in the cement. The conditions are not unlike those in a 
cavity of simple depth and to the mind of the writer do not necessitate 
devitalization before crowning, as most of the pulps live unless danger- 
ously approached in grinding. When trouble from nodules has arisen 
in the writer's practice it has occurred in teeth previously abraded. 
Reference to Fig. 337 will show why grinding may cause undue pulp 
24 



370 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

approach or stimulation to be added to an already stimulated pulp. 
Nodules are found much more frequently in the teeth of middle- 
aged persons than in those of youth, although they may be present 
as early as the ninth year, as shown by radiography. They occur 
more frequently multiple than single. Some of the larger nodules 




PN 



A pulp nodule fused to the parietes of a pulp cavity. Prepared by grinding: PN, 
pulp nodule; D, dentin of the tooth. X 15. From section by J. F. Colyer. (Hopewell- 
Smith.) 



are evidently formed by the coalescence of smaller ones. The num- 
ber in a single pulp varies, usually from one to three or four but 
occasionally more. With a number of teeth involved a considerable 
aggregate may exist in a mouth. 

Pathology and Morbid Anatomy. — The structure of pulp nodules 
does not resemble that of dentin; they possess about the same degree 



PULP NODULES 



371 



of translucency and hardness as secondary dentin and at times may 
have opaque portions. This characteristic is also true of secondary 
dentin and.hypercementosis and may represent merely the whimsical 



Fig. 344 




Section of a pulp nodule, showing many calcospherites, as pointed out by a, a. (Black.) 

variations in calcoglobulin make-up or in histological forms as seen 
in the varieties of secondary dentin. Outwardly they may assume 
almost any form; they range in size from minute bodies to a size 
sufficient to almost obliterate the pulp (Figs. 340 and 346). 

Fig. 345 




Deposit of calcoglobulin within the tissues of an inflamed pulp. (Black.) 



A section of a nodule exhibits the presence of a number of concen- 
trically laminated bodies, recognizable as hardened calcospherites. 
Black found them to rarely make up any considerable portion of the 
bulk of the nodule. The remainder of the nodule is made up of 



372 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

structureless material which may contain a few fine tubes, considered 
by Hopewell-Smith as produced by the long fusiform cells. 

Black also found deposits in the pulp which throw light upon the 
possible origin of nodules in some cases, and to some extent upon 
the conditions under which they may be formed. In the pulp of 
a second molar of a girl, aged fifteen years, in which there had been 
decided subjective evidences of pulpitis recurring at intervals for a 
period of two months, he found a mass representing a pulp nodule in 
its soft state. " About one-half of the coronal portion of the pulp was 




Calcification of the dental pulp: At A is shown the outline of a lower molar with a 
cavity at &. The pulp chamber is much reduced in size and filled with calcific material, 
as shown in B. a, a, large granular mass of calcific material, which is very transparent, 
but finely granular. A very few irregular lines are seen in the centre, which slightly 
resemble dentinal tubes; b, an erratic growth of irregularly formed and unusually 
transparent dentin; c, line of the growth of dentin from the floor of the pulp chamber — 
the growth from other directions is so perfectly regular as to leave no markings; d, 
margin of the cavity of decay; e, a bundle of cylindrical forms of calcific material 
extending down into the root canal. These extended to the apex of the root. (Black.) 



involved in the inflammation; lying a little inside of the layer of 
odontoblasts were several masses similar to Fig. 345, having globular 
forms in their mass or attached to their margins. The globular 
bodies present the laminated appearance of calcospherites." These 
masses may in all probability be interpreted as intermediate products 
in the formation of nodules; they have not yet become calcified. 

A small nodule may be made up of laminated, structureless 
material, the laminae being arranged about a central nucleus, the 



PULP NODULES 373 

nature of which is not clear, but may possibly be calcified dead cells 
(Fig. 347). 

The conditions of calcification of nodules are not definitely known. 
Hopewell-Smith 1 considers that they are deposited by the pulp cells as 
a secretion about themselves, and that the cells are later obliterated 
or may persist in situ (Fig. 348). He also describes and illustrates 
a case of a nodule which had within it a pulp cavity containing 
pulp tissue. 

Pulp nodules occur, as a rule, in the better grades of teeth which 
show constructive tendencies upon the part of the pulp. 

Fig. 347 




A pulp nodule isolated from the pulp. Shows its central nuclear formation and 
its concentric lamination. Prepared by grinding. X 50. From collection of G. W. 
Watson. (Hopewell-Smith.) 

It is probable that in these pulps the pulp cells under conditions of 
irritation secrete calcoglobulin, which in part is developed into spher- 
ites and in part remains without definite histological characteristics. 
This is not surprising when we consider the spherites and amorphous 
cement substance of which dentin and enamel are built up. The 
masses are probably calcified after their deposition. Whatever the 
origin of the masses — by cell secretion or otherwise — the histological 
record indicates a gradual increase in the size of the deposit. Pres- 

1 Normal and Pathological History of the Mouth, 1918, ii, p. 20. 



;}74 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

sure upon the nerves results in irritation and an increase in pulp 
hyperemia which causes the reaction to thermal changes. Pulp 
nodules are usually found in the coronal portion of the pulp, but 
sometimes exist in the root portions, either free or embedded in 
secondary dentin. If they obstruct the lumen of the canal they 
cause interference with the circulation and nerve tissue and may 
produce great pain or pulp death, probably through profound arterial 
followed by venous hyperemia. Bunting calls attention to the pos- 
sibility that the nodule moving freely in the pulp may allow arterial 
pressure to raise it, permitting blood entrance, while the venous 
pressure may return it to place and prevent exit of blood thus induc- 
ing continued internal pressure in the pulp (a venous hyperemia), 
thus causing functional disturbance and pain. 1 As in the case of 
secondary dentin, nodules may be produced by reflex hyperemia, as 
they are quite frequently found in teeth near to an impacted tooth. 

Fig. 348 



PN 




MN 



• Sr-PN 



MN 



The formation of the pulp nodule. Prepared by Mr. Hopewell-Smith's process. 
PN, pulp nodules; MN, medullated nerve bundles; T, pulp tissue; C, capillary. 
X 230. (Hopewell-Smith.) 

Symptoms. — Multiple nodules may exist in a dental pulp and give 
rise to no evident symptoms whatever, as is shown by their presence 
in extracted teeth, many of them free from caries, and in which there 
was no history of pain. On the contrary, the pulp of a tooth may 



1 Dental Cosmos, February, 1912, p. 169. 



PULP NODULES 375 

react persistently to thermal changes or even be the seat of intract- 
able pain without a depth of carious invasion which would lead to 
the inference of acute pulp disease; and relief only be secured 
through devitalization of the pulp, which upon examination may 
reveal a small or large pulp nodule. 

The symptoms attendant upon the presence of nodules, so far as 
they can be made out, appear to be of two types — those associated 
with small and those with extensive deposits. Reflex pain is the 
common associate of both. 

Small Deposits. — While it is true that pulp nodules may often 
exist in apparently sound teeth without inducing pain, yet the 
pulps of teeth containing them may become excessively hyperesthetic 
under what are ordinarily mild sources of irritation. This is mani- 
fested, first, through the contents of the dentinal tubuli; the dentin 
becomes exquisitely sensitive and cool water directed into a shallow 
cavity produces a paroxysmal and excruciatingly painful response 
from the pulp. In the absence of direct, extraneous irritation of the 
pulp, the dental symptoms may be absent, but a persistent, possibly 
intermittent, neuralgia may be located at some distant point. Pain 
in or about the ear is a frequent symptom. Occasionally an obstinate 
scalp neuralgia, with the existence of a hyperesthetic spot, appears. 
Pain in the eye, with tenderness over the supra-orbital foramen, is 
also common. Guilford 1 has reported a case of tic douloureux of two 
years' standing, the result of pulp nodules. The pain may be recurrent 
or persistent. The results of neuralgic pain and loss of sleep conse- 
quent thereon, may have serious effects both mental and physical. 
Fortunately in a single practice these results are not so frequent. If 
arsenical applications be made to devitalize the pulp, it is found that 
not only is intense pain often caused, but examination after even a 
week or more shows the pulp to be still vital and hypersensitive; and, 
in order to effect its destruction, repeated applications of arsenic 
must be used. Pressure anesthesia or cataphoresis also is apt to be 
slow in action. 

Large Deposits. — In extensive deposits of pulp nodules the 
dentin may be almost devoid of sensation, and applications of heat 
or cold, even in large cavities, may be followed by delayed and faint 
pulp response. Such cases, however, commonly give a history of 
reflex neuralgia and vague dental pains extending over a period, it 
may be, of years. With some large deposit the pain in the pulp may 
take an opposite course and be exquisite. 

Diagnosis. — Their diagnosis by means of the z-rays is positive 
(Figs. 349, 350, and 351), but their diagnosis by symptoms may only 

1 Private Communication. 



376 CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

be inferential and confirmation be lacking until after devitalization 
of the pulp and the finding of the pulp nodules in its substance. 

The tardy action of arsenic is also observed in the cases of large 
deposit, it being frequently necessary to devitalize the pulp piece- 
meal, and sometimes the arsenic will hardly be tolerated at all. 

Treatment. — Pulps inferred or shown by z-rays to contain nodules 
should be removed if symptoms demand it. If discovered only in 
course of radiography they may be ignored. Considering the possible 
difficulties and the time consumed the best method seems to be con- 
ductive anesthesia under which the entire pulp may be removed 
almost at leisure. In anterior teeth for the same purpose nitrous 
oxid and oxygen may be used or in selected cases even the ordinary 
N2O apparatus. Either of these or pressure anesthesia in some 
form may be used to aid removal of the pulp bulb and obtain blood- 



FlG. 349 



f 



Fig. 350 



iFig. 351 





Pulp nodules in the radicular and 
coronal portions of the canal. (Radio- 
graphs by Price.) 1 



First and second bicuspid roots 
filled. Pulp nodule in first molar. 
(Radiograph by Lodge.) 



letting after which arsenic may be used perhaps repeatedly as the 
pulp is resistant in some of these cases. In old days eighteen months 
was required in one case. (See Chapter on Removal of the Pulp.) 
Ottolengui 2 suggests for difficult pressure anesthesia cases the repeated 
applications of ether on cotton, until no pain follows, leaving the 
last pellet, spraying with ethyl chlorid, removing the cotton and pro- 
longed spraying again as valuable in removing the calcifications. 

If the nodule be found as a spicular deposit in the mouth of the 
canal, it may usually be removed by teasing it from side to side, 
first soaking the part with a sodium hydroxid solution, or 50 per cent, 
sulphuric acid, which quickly destroys the organic matter of the pulp. 

Pericemental reactions are quite apt to follow the removal of such 
pulps. This result is best obviated, if arsenic is used, by awaiting 
the thorough death of the pulp filaments before attempting their 



1 Items of Interest, 1901. 

2 Dental Items of Interest, June, 1918, p. 494. 



CALCIFIC DEGENERATION OF THE PULP 



377 



removal. Of course, other methods are available, but reactions still 
may occur. It seems as though a habit of irritability were established 
in the tissues. For this reason, after pulp removal, it is well to seal 
a cotton dressing with campho-phenique plus menthol as a sedative 
for a time. Count erirritants may be applied to the gum. (See 
Non-septic x4pical Pericementitis.) 

Calcific Degeneration of the Pulp. — By calcific degeneration is 
meant the infiltration of inorganic matter derived from the lymph 
into tissue which is dead or undergoing degeneration. It occurs in 
any part of the body in which the necessary conditions are present. 

Cause and Pathology. — The conditions apparently necessary for 
the production of calcific degeneration are those which occur in a 
semistagnant blood current. An acid reaction occurs owing to the 
presence of an excess of carbon dioxid and catabolic products, which 
favors deposition of inorganic matter. The albuminous matter of 
the tissue undergoes degenerative changes owing to the faulty nutri- 
tive supply and waste removal. (See page 62). 

Fig. 352 




A, outline of a lower molar, with a large carious cavity at a; b, pulp chamber; 
the shaded portion, c, was occupied by cylindrical calcifications. B, cylindrical 
calcifications. X 100. (Black.) 



Probably some cells die. They or their constituents have some 
affinity for inorganic salts which are taken up from the lymph. Thus 
gradually the tissue becomes infiltrated. 

Those causes which produce a sufficient degeneration of pulp tissue 
to induce the above process are: (1) The pulp exhaustion due to 
the formation of secondary dentin or pulp nodules; (2) continued 
hyperemia or chronic inflammation in which venous hyperemia plays 
a part. 

The calcific material, unlike the cases of nodular calcification, 
encloses the anatomical elements of a pulp in process of degenera- 



CONSTRUCTIVE DISEASES OF THE DENTAL PULP 

tion in a mass produced by deposition, not secretion. In the root 
portions of pulps in which fibrous elements have become pronounced 
the calcification may be tubular or cylindrical in character, the 
nature of the calcareous masses being apparently a deposition 
about and along the fibers (Fig. 352). 

Upon optical examination the masses are seen to be opaque, are 
brittle, and decidedly unlike pulp nodules in form. They may be 
associated with pulp nodules as an added and more advanced degen- 
eration. The nodules may also have opaque' portions attached to 
the clearer masses (see page 371). The pulps are, of course, living. 
There is a comparative absence of cellular elements in the pulp — 
i. e., they have atrophied, degenerated, and been absorbed. 

Another evidence of the cellular degeneration is seen in the great 
ease with which such pulps are removed after devitalization, even 
the most minute apical portions freely coming away after slightly 
catching a hook in the pulp — i. e., the usual odontoblastic 
attachment to the dentin is not present. When extracted these pulps 
have a granular feel to the fingers, and when dry may be quite stiff 
(Fig. 353). _ 

Fig. 353 illustrates a case discovered upon fracture of a molar 
during the operation of extraction. In another case the pulp was 
slightly bendable when extracted, but after drying for a half-hour 
became at its apical end of needle-like sharpness and stiffness. It 
was filled with calcific granules. 

Symptoms. — Degenerations of the pulp, as a rule, present symptoms 
of reflex pain, vaguely referred to other parts. The response to hot 
applications is usually greater than that to 
Fig. 353 co \^ ones? an d both are delayed — i. e.) five 

seconds or more may elapse before pain 
follows a severe test like the intensely cold 
spray of ethyl chlorid or a hot copper ball 
or blast of hot air. At times with an open 
pulp chamber the symptoms of chronic 
pulp inflammation are obtained. There 
may be a painful reaction to arsenic applied 

Lingual filament of pulp {-Q -j-J^g pulp. 
of an upper molar, broken tr y 

in extraction. The rigidity Diagnosis and Treatment. — I he z-rays may 
of the filament was due to afford a positive diagnosis if some nodular 

the presence of calcific . , , ", . . , 

granules. mass be present, but probably not in the 

more granular forms as detail will be lacking 
in the radiograph. In such cases the diagnosis, apart from the infer- 
ence from the symptoms, is a postmortem one. In cases warranting 
the interference, in which there is a delayed response to intense ther- 




CALCIFIC DEGENERATION OF THE PULP 379 

mal tests applied to a filling or a clean pulpal wall, the pulp should 
be removed and may then be found to contain the granular masses. 

The constructive diseases of the pulp are an evidence of an attempt 
upon the part of the pulp to protect itself; but with the exception, 
perhaps, of a very regularly deposited secondary dentin the effects 
react upon the pulp itself, causing its destruction. To what extent, 
therefore, secondary dentin is beneficial is an open question. 

Evidences of constructive action upon the part of the pulp may 
occasionally be noted in the temporary teeth — e. g., secondary dentin 
following deep abrasion. 

There do not seem to be any observations as to the formation of 
nodules or calcific degenerations in the pulps of temporary teeth, but 
there is no good reason why they should not occur, particularly after 
abrasion. The pulp diseases of the temporary teeth are usually of 
an acutely destructive nature, which may account in some degree 
for the absence of reports touching this subject. 



CHAPTER XIII 

DESTRUCTIVE DISEASES OF THE DENTAL PULP 

The pulp diseases classed under this heading are those vascular 
disturbances which, in more advanced stages, tend to bring about 
death of the pulp. In the earlier stages, if maintained, either con- 
structive changes or degenerative partial stases occur, which may 
again lead to calcific deposits. It will, therefore, be noted that the 
constructive changes may lead to the destructive forms of vascular 
disturbance owing to their presence, while in turn the vascular 
changes may lead to constructions if the degree of disturbance neces- 
sary be maintained. 

HYPEREMIA OF THE PULP. 

Hyperemia is an excess of blood in the more or less dilated vessels 
of a part. It is of two forms: Active or arterial and venous or 
passive. These differ in the manner of causation and in their effects. 

In inflammation both arterial and venous hyperemia occur, together 
with the characteristic emigration of leukocytes and exudate of coagu- 
lable lymph, but neither of the forms of hyperemia have these to any 
extent and therefore they are not inflammation (see page 34, etc.) 

Arterial Hyperemia of the Pulp. — This is an excess of blood in 
the dilated arteries and capillaries of the pulp, the pulp functions being 
increased in the mild continued cases and disturbed by a gradual 
passage into venous hyperemia in the more severe cases. 

Pathology and Morbid Anatomy. — The bloodvessels are under the 
control of the vasomotor nerves derived from the sympathetic sys- 
tem and which respond, as a reflex, to irritation of sensory nerves, 
through their relations with them at sensory centers, by causing 
dilatation of the arterioles. This dilatation is due to a decrease in 
the control of the caliber of the vessels through relaxation of the 
circular muscular fibers, i. e., the muscular tone is lost in proportion 
to the irritation (Fig. 7). In proportion to the loss of tone, the vessels 
become more enlarged and tortuous and in marked cases exhibit 
aneurysmal enlargements due to the pressure (Fig. 359). It is prob- 
able that a degree of venous hyperemia is associated with the pro- 
duction of this state of the vessels and as it becomes more pronounced 
(380) 



HYPEREMIA OF THE PULP 381 

the condition of a fully developed venous hyperemia is established 
(see page 393). 

The functions at first increased are later diminished in proportion 
to the venous hyperemia present. Owing to the peculiar anatomy 
of the pulp cavity no sharp line can be drawn. 

In arterial hyperemia the pulp can recover its tone and even with 
considerable venous hyperemia it may do so, but the recovery is 
less likely especially if the action of the exciting cause cannot be pre- 
vented. Outside of these microscopic phenomena nothing remarkable 
occurs. 

Degrees of Arterial Hyperemia. — It is plain from the foregoing and 
from the clinical expressions of this condition that every grade of 
arterial hyperemia from the pure, mild, arterial form to a mixed 
arterial and venous and finally to a profound venous hyperemia may 
result if a cause be sufficient and continue its action. Three grades 
may therefore be established: 

1. A very mild form without noticeable symptoms and associated, 
as a rule, with long-continued stimuli and with constructive effects 
as described under secondary dentin, etc. 

2. A mild form exhibiting increased irritability expressed in a 
reaction to thermal shock as a slightly painful response passing away 
promptly. This form is usually due to causes of reasonably acute 
nature though sometimes due to the later effect of constructions, 
e. g., secondary dentin or pulp nodules. 

3. A more severe form, usually the result of the action of causes 
acting more powerfully or to the continuance of the causes producing 
the second grade which passes into the third. In this grade thermal 
shock usually produces more violent response, shocking a pulp 
already irritated by thermal or other irritants, and reflex pains, to 
be described later, are apt to occur. 

Causes and Symptoms. — The consideration of the primary causes of 
arterial hyperemia is of great importance as often their removal is 
the only treatment necessary for the recovery of the pulp and pulp 
removal may be avoided. The diagnosis may often be confirmed by 
the therapeutic test. They may be classed as direct and indirect. 

1 . Direct Causes. — A direct cause is one acting upon the pulp by 
way of the crown of the tooth. The mode of action of the causes 
may be divided into: 

(x) Direct and immediate action upon a pulp. 

(y) Direct action upon the fibrils rather than the pulp. These 
being irritated,, the irritation is transferred in turn to the odonto- 
blasts, the sensory nerves, the sensory center, the sympathetic nervous 
center, which via the vasomotor nerves, furnishes the motor reflex 



382 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



relaxing the muscular fibers and causing dilatation of the arterioles, 
which permits the overfulness of the vessels, establishing arterial 
hyperemia. This action requires a day or two to produce symptoms 
or may merely produce a first-grade hyperemia (see above). 

I.t. Direct Immediate Causes. — These are: 

(a) Thermal shock chilling or heating a pulp immediately through 
a cavity of decay which removes the non-conducting covering of the 
pulp (Fig. 354). 



Fig. 354 



Fig. 355 



Fig. 356 



Fig. 357 




Fig. 354. — A, Cavity or metal filling approaching pulp: B, hyperemic (sometimes 
inflamed) pulp; C, area of hyperemia of apical tissue, due to extension from the pulp 
or possibly to back pressure of blood. 

Fig. 355. — A, Area of non-septic inflammation of apical tissue due to injury as 
from a blow or malocclusion; B, hyperemia or mild non-septic inflammation of the 
pulp due to overflow from the apical tissue. 

Fig. 356. — A, pyorrhea pocket; septic inflammation at C; B, area of lesser inflam- 
mation (non-septic); D, hyperemia of pulp; E, normal tissue. 

Fig. 357. — A, ulcerated or necrotic alveolar wall due to injury and infection; B, 
inflammation more or less non-septic (lesser inflammation) ; C, hyperemia of pulp 
due to overflow of blood at B. An abscess on an adjoining root has the same pathology. 
If extending to the molar it infects its pulp from the apex. (See pages 39, 40, and 45.) 



(b) A metal filling placed too close to a pulp without sufficient 
non-conducting intermediate filling material. 

(c) A pulp nodule previously caused b}' some mild irritation may, 
through its presence, excite a more severe irritation and hyperemia 
and thus be a cause under this heading. (See Pulp Xodules.) 

(d) The action of galvanism, either induced by unlike metal fillings 
as a sudden shock, or by a galvanic battery as in cataphoresis (or 
ionization) or the action of electrolysis, a possible occurrence in cata- 
phoresis. This will be considered separately (see pages 329 and 387.) 

In these cases the cause acts rapidly, the pulp reaction is prompt 
and the hyperemia may become so marked that very slight changes 
of temperature cause painful shocks. The pain, usually lancinating, 
may later not be felt in the pulp, but be reflected to other localities, 
e. g., the gum above or between the teeth, another tooth, the ear, 



HYPEREMIA OF THE PULP 383 

the eye, the supraorbital region, the infraorbital region, the chin, 
scalp, arm, etc. 

As a rule, when an upper tooth is affected the pain is located along 
the branches of the superior maxillary division of the fifth nerve; 
if a lower, along the branches of the inferior maxillary division. 
They may appear in other branches, however. 

It varies from vague uneasiness to an acute neuralgic attack, with 
tender spots over the foramina of emergence of the nerves. 

It is perfectly possible that an exposed pulp may experience these 
shocks and may be simply hyperemic, but this cannot be distinguished 
clinically from a pulp infection and inflammation so that the latter 
condition may, for clinical purposes, be regarded as pulpitis, while 
up to actual exposure hyperemia may be considered at least tenta- 
tively until the therapeutic test is applied. 

ly. Direct Causes Acting through the Fibrils. — The causes acting in 
the manner described above (page 381) are: 

(a) Thermal shocks delivered to exposed dentinal fibrils at (1) the 
cervices of teeth, whether decalcified or not; (2) upon abraded, eroded 
or fractured surfaces; (3) in shallow cavities and upon metal fillings 
placed in shallow cavities. 

(6) The bruising of the cut ends of dentinal fibrils, through forceful 
placement of gold, amalgam or other fillings against them. A mild 
reaction is frequent, a severe one occasionally results. 

(c) The chemical irritation of the fibrils in cavities or under crowns 
by cements, cavity contents, or the infiltration of salt, sweet or acid 
substances into contact with the fibrils exposed in any location. 

(d) Irritation of fibrils by septic saliva beneath a leaky or loose 
filling or septic dentin left under fillings, or septic cement under a crown. 

In these cases the pulp becomes hyperemic and usually after 
several days the tooth responds to thermal shock as a mild pain 
passing promptly, as a rule. This proves the gradual .onset of the 
condition. 

It is surprising to what an extent the pulp may protect itself 
against thermal stimuli through the formation of tubular calcifica- 
tion and secondary dentin, and even in quite deep cavities, this 
gradually produced hyperemia generally passes away in a few weeks. 
Theoretically a calcoglobulin plasma is exuded which protects the pulp 
and brings about a toleration. (See page 360.) 

In the case of exposed hypersensitive cervices, which have permitted 
a general pulp hyperemia, shown by the reaction to cold, applied 
anywhere . about . the tooth, application of silver nitrate or other 
obtundents to the sensitive fibrils, reduces the hyperemia if not com- 
plicated by other conditions (pulp nodules, etc.). 



384 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

In the cases in the fourth class (1 y-d) the correction of the condi- 
tion may permit a comfortable refilling, with antiseptic fillings, under 
proper conditions, though this depends upon the cavity depth and 
the duration of the sepsis. 

As an example of a case of class (1 y-b), a molar with very small 
distocervical cavity reacted but slightly to burring, but twice pro- 
duced such prompt, sharp and continued response to the pressure 
of ordinary amalgam insertion as to compel immediate removal and 
sedation for several days, after which a gentle filling was tolerated. 

Gold pounded into shallow cervical cavities has occasionally pro- 
duced a hyperemic reaction referable either to the same class of 
mechanical fibril irritation or thermal irritation. 

2. Indirect Causes. — The indirect causes are those (a) acting through 
the pericementum or (6) through reflex action from parts other than 
the affected tooth itself. These may be subdivided into — 

1. Inflammation or hyperemia produced in the apical tissue by 
trauma or bruise, the result of a single violent blow or of repeated 
blows as from malletting, malocclusion, thread-biting, etc. (Fig. 355). 

2. Irritation produced by hypercementosis, itself a result of a 
hyperemia of the pericementum. 

3. Inflammation or hyperemia of the apical tissue of the hyperemic 
tooth, the result of extension of the hyperemic or non-septic inflam- 
matory zone (lesser inflammation) of a nearby inflammation into the 
said apical tissue (Fig. 357). 

The specific causes of this third class of indirect causes are: 

(a) An abscess on an adjoining tooth (Fig. 357 will illustrate). 

(b) A fairly deep pyorrhea pocket on the tooth or on the next 
tooth (Fig. 356). 

(c) An ulcerated alveolar process resulting from the use of alveolar 
forceps, bruising from a hypercementosed tooth or infection, or even 
the normal healing inflammation in an alveolus (Fig. 357). 

(d) An aphthous ulcer upon the gum over the tooth. 

The mode of action is first the production of apical hyperemia, the 
excess blood from which flows into the pulp, causing its hyperemia. 

A practical example : 

The writer received a slight blow on a sound lower incisor. On 
the second day thereafter the tooth was tender to touch and responded 
to cold. It was shielded and after two or three days was normal 
to touch and to cold applications. This was a class 2, Xo. 1 case. 

It is possible that the irritation may be in part the result of reflex 
vasomotor disturbance, either beginning with apical pulp irritation 
in the tooth or at the area of original inflammation, thus: Area of 
injury, brain center, reflex to the tooth pulp. (See 2 (b) } next page.) 



HYPEREMIA OF THE PULP 385 

In these cases the primary cause may be septic or non-septic, but 
in either case the pulp hyperemia is considered aseptic unless the 
septic zone comes too near the apical foramen in which case the 
condition becomes one of pulp infection and inflammation. (See 
Pulpitis.) 

2 (b). Reflex Action. — An inflamed or intensely hyperemic pulp in 
one tooth may have its brain response transferred to another pulp. In 
operation the sensation from the first pulp is carried to the sensory 
center and either the pain may be transferred to the other pulp 
(reflex pain) or a vasomotor reflex may be directed into the second 
pulp producing a hyperemia (reflex action). The second tooth pulp 
reacts to cold as usual. 

The cause in the first tooth, if suspected or discoverable, should be 
removed, and if the reaction in the second subside a diagnosis of 
arterial hyperemia by reflex is confirmed, and the second pulp 
requires no treatment. This reflex to other pulps is well known. 

A practical example showing this result occurred to the writer. 
A lower third molar was extracted. The alveolus healed gradually 
with some local irritation. A localized scalp tenderness supervened 
which passed with the final healing of the tooth socket and due, 
without doubt, to vasomotor disturbance in the scalp by a reflex. 

In another practical example an upper bicuspid responded annoy- 
ingly to cold. It had been well filled for twenty years. Examina- 
tion revealed a large new amalgam filling on the buccal of the third 
molar. A history of pulp devitalization was given. The pulp was 
found half dead, the apical half highly inflamed. Its removal cured 
the reflex hyperemia in the bicuspid. 

In another case an almost exposed pulp in an abraded cuspid pro- 
duced marked reflex to a sound molar which responded to cold, the 
cuspid giving no pain. The hyperemia in the molar was cured by 
removal of the cuspid pulp. 

Irritation of branches of the fifth nerve as by common cold, 
influenza, malaria, syphilis or tumors may produce an identical reflex 
to a tooth pulp, causing pulp hyperemia which passes with the 
general disease if cured. There is evidence that some pulps so 
irritated die. Irritations in other parts as the uterus, bladder, etc., 
may at times, in like manner, have the irritation reflected, via the 
brain center, to a tooth pulp, causing pulp hyperemia. 

Idiopathic Hyperemia. — In some cases with sound teeth no obvious 
cause can be found, as a history of thread-, nail- or cigar-biting, etc., 
as evidence of cause and patients may deny even so simple a true 
fact. This may be borne in mind. Perhaps the case is one due to 
infarctions or pulp nodules, etc. Lower incisors are particularly 
25 



3S6 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



prone to it. The tooth responds markedly to thermal -changes and 
while the cause may not be obvious or obtained by history or radiog- 
raphy it might really fall under the previous classifications if it 
could only be obtained. 

Xodules may possibly be discovered by radiography or by examin- 
ing the pulp after extirpation, rolling it in the fingers. In some 
marked cases, however, no cause could be discovered, though micro- 
scopic examinations were not made. It may.be that some form of 
septic transference from some other focal infection may account for 
the hyperemia. (See Rosenow's Experiments Under Pulp Gangrene.) 




Hyperemia of the dental pulp, showing the injection of the vessels: a, a, mem- 
brana eboris, or layer of odontoblasts; b, b, b, b, vessel distended with blood: c, c, c, c, 
points from which the blood has fallen in handling the section. (Black.) 

Hartzell and Henrici 1 are of the opinion that bacteria may enter 
the pulp from the gum margin by way of the pericemental channels 
or be transferred from abscessed teeth several teeth away as they 
claim to have found them on examination. Regardless of cause the 
pulp must be removed. 

There are some individuals nearly all of whose sound teeth are 



Journal of the National Dental Assn., May, 1917, p. 493. 



HYPEREMIA OF THE PULP 



387 



sensitive to thermal changes sometimes for life. Whether this is due 
to some abnormal sensitivity of pulp tissue or to the thinness of the 
enamel and dentin overlying it is not clear. 

Pulp Irritation from Electric Action. — It is of quite common occur- 
rence that galvanic electricity causes pulp irritation. The cataphoric 
current too long continued may induce a hyperirritability of the 
pulp amounting in some cases to evidence of hyperemia, which 
may subside under proper treatment or eventuate in pulp death from 
venous hyperemia. The occasional connection of a newly placed or 
bright amalgam filling with a gold filling, bridge, plate, or clasp, 
through the medium of saliva or food (which amounts practically 
to the same thing), will, at times, produce painful galvanic shocks in 
a vital tooth. Dr. Franz Trauner 1 has reported that such pain has 

Fig. 359 




Dilated bloodvessels from the dental pulp in hyperemia, from tooth extracted during a 
paroxysm of intense pain. (Black.) 



been felt in devitalized teeth. This is outside of the editor's experi- 
ence, and should not occur in totally devitalized teeth, as the electric 
current is a test for pulp vitality. I have later noted a case of shock 
in a vital left upper bicuspid filled with amalgam opposed by a dead 
left lower bicuspid with gold crown after insertion of amalgam in a 
right lower tooth. It occurred only when the mouth was closed and 
was felt as though in the lower left tooth. Dr. Paul Manning 2 
recounts a case in which gold placed entirely over a substratum of 
old amalgam filling produced intolerable pain which was relieved by 
drilling through the gold to the amalgam and filling the drill hole 
with amalgam, thus bringing both into contact with the oral fluids. 



See Dental Cosmos, 1903. 
Dental Cosmos, 1918 p. 29, 



3SS DESTRUCTIVE DISEASES OF THE DENTAL PULP 

The mouth mirror, or a fork or pin, or a brass depressor touched to 
a new amalgam filling, may also produce the pain, but a nickelled steel 
instrument usually does not, but may connect mirror and filling. 

Painful shock is sometimes produced by the animal electricity 
discharged from the operator during dry, cold weather. It usually 
occurs when the finger is placed upon a metal filling, or the plugger 
point is returned to a metal filling. Touching the metal part of the 
chair before approaching the patient will obviate this disagreeable 
contact. 

Treatment. — With cataphoresis, the mischief being accomplished, 
the case must be treated as other arterial hyperemias. 

In the case of shocks from the presence of the two metals it may 
be ignored if slight and the filling new, as it will probably soon pass 
away. If the fillings be in adjoining teeth, they should be contoured 
so as to touch persistently if possible. If in the same tooth, the 
fillings should be connected by either amalgam or gold. A well-set 
and brightly polished amalgam filling may be tarnished if necessary 
by touching it with a 1 per cent, solution of silver nitrate; or, if 
good color be a necessity, the pulp of the tooth may be well in- 
sulated by means of a gutta-percha substratum, or the pulp may 
be devitalized. 

Associated Hyperemia of Pericementum. — In all pronounced pulp 
hyperemias and inflammations (which latter are hyperemic conditions 
also) some of the excess blood may find its way into the apical tissue 
and cause apical hyperemia with symptoms of tenderness to tapping 
upon the tooth or even to touch (Fig. 354). 

In a rare case of a lower cuspid with small labial cavity filled with 
a silicate cement, a class ly-b, direct cause, produced arterial hyperemia 
and a persistent mild tenderness to touch without a corresponding 
reaction to cold. It was relieved by refilling with oxid of zinc and 
eugenol cement for a few weeks. Later, after varnishing the cavity 
floor, the silicate was replaced without further irritation. 

Diagnosis. — When a tooth pulp responds to thermal stimuli, espe- 
cially to moderate heat or cold, hyperemia or inflammation (also 
hyperemic) is inferred. Assuming the response to be in a tooth 
without pulp exposure, and not too long continued, a direct cause in a 
cavity, recent metal filling, etc., hypersensitivity at cervices, sepsis 
under filling, etc., as shown above, is first sought, and if found, cor- 
rected, as for example, by sedatives on cotton in a cavity, sedative 
filling, etc., permanent filling, if indicated, silver nitrate to hyper- 
sensitive necks, etc. Direct causes not being discovered, indirect 
causes or reflexes are sought and removed or treated. 

Failing an apparent acute cause, filled teeth are tested to determine 



HYPEREMIA OF THE PULP 389 

the hyperemic pulp and the filling removed to discover, if possible, 
any condition causing inflammation with which arterial hyperemia is 
always associated (see Pulpitis, etc.), or possibly septic dentin may 
be present under the filling as a cause of hyperemia. 

Whether as a cause of hyperemia or inflammation is judged by 
the degree of approach to the pulp and the response to treatment. 

In testing a reflex to a pulp or to some other part, the suspected 
tooth is subjected to drop after drop of cool or cold water as indicated 
in the endeavor to cause an acute paroxysmal response. 

In testing to determine which of several teeth contains the hyper- 
emic pulp two methods are employed : 

1. The head is thrown well back so that the water runs into the 
throat. Then drop by drop cold water is thrown on the most posterior 
tooth. Time is allowed for effect. None resulting, it is then dropped 
upon the tooth next anterior, and so on, until a sensitive tooth is 
found. 

2. A square or full piece of rubber dam with a single hole is passed 
over one tooth and the cold-water test applied. Heat in the form of 
hot gutta-percha, hot air, etc., may be used. If two teeth only are 
in question and the dammed one excluded the dam is then folded 
over the excluded tooth and the water thrown on the other. If 
several teeth are under suspicion each is dammed in turn and tested. 
In some cases a piece of lubricated dam is run between the teeth 
and may be folded over one or the other. 

As stated, the location of a hyperemic pulp does not alone warrant 
its removal. The appropriate cause must first be considered. 

Idiopathic cases are different, which see. 

The electric diagnostic lamp shows the pulp engorgement in some 
of the advanced cases. 

Radiography is useful in occult cases as a means of diagnosing 
pulp canal constriction by secondary dentin or pulp nodules. 

In advanced cases responding markedly to thermal changes, a 
history of a deep filling, pressure pain at the time of filling, etc., is 
evidence to be considered in making up a diagnosis. In such cases 
the hyperemia is usually progressive toward the venous variety and 
frequently not the slightest thermal change is tolerable. 

Prognosis. — The prognosis is good for all moderate cases if the 
action of the causes can be prevented, as pulp may recover its tone. 
(See page 380.) In flat abrasions with the pulp nearly exposed, it is 
unfavorable. In fractures not exposing the pulp, caps may be used 
to advantage, especially in children's teeth. Pure gold crowns may 
be used until such time as the pulp canals are complete, though 
pulp removal may or may not be required for the final restorations. 



390 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

• 

In pulp capping cases the prognosis is not good, but unless the 
reaction is severe and if it grows less gradually under counter- 
irritation, success may be hoped for. 

(Treat reactions to thermal shock in deep cavities offer a rather 
unfavorable prognosis, but an effort to save through sedation may 
be made unless there be no room for non-conductors. 

Treatment. — Open cavity cases require the exclusion of the causes, 
usually sepsis and other chemical irritants and thermal stimuli. 
In some cases the pulp must be sedated to allow the vessels to recover 
their tone. Filling with these points in mind, i. e., asepsis, non- 
conduction and permanence is indicated. (See Almost Exposed 
Pulp.) 

In the most doubtful cases, with deep cavity and great irritation, 
sedatives applied on cotton for a few days are indicated. The cavity 
is excavated as far as possible and the application renewed, at least 
daily, either by the operator or patient until sedation is accomplished. 

In somewhat less doubtful cases, oxyeugenol plus a trifle of thy- 
mol may be used as a temporary filling to be later entirely or 
partially removed, or Jodof ormagen covered by oxyeugenol may be 
used. As a preferable alternative Jodoformagen may be placed in 
the pulpal wall of the cavity and a soft, quick-setting cement plus 
thymol flowed over it as a cavity lining, over this, when set, a gutta- 
percha base plate is to be placed to fill the cavity temporarily. 

In moderate cases the cavity may be touched with oil of cajuput, 
etc., and gutta-percha introduced as a temporary filling. 

In simpler cases a permanent combination filling of cement plus 
thymol and amalgam (if indicated) may be used, or the cement lining 
may be used with gold in view. The cement plus thymol may be 
placed to be partly cut out later, or a gutta-percha intermediate may 
be covered with cement and amalgam (or later gold may be used 
instead) . 

The indications vary with the cavity depth and the degree of 
irritation, and in some cases may require temporary filling with 
gutta-percha or cement for some time. 

In all cases of very deep cavities non-conductors must be placed 
as a prophylactic against thermal shock. This may consist of var- 
nish, or a layer of gutta-percha base plate. In general the writer 
prefers the Jodoformagen and thymolized cement above mentioned 
as fulfilling immediate and subsequent requirements. 

When hypersensitive cervices are the cause of the pulp irritation 
several applications of silver nitrate, at intervals of a few days, will 
usually reduce the hyperemia in a few weeks. The fibrils are super- 
ficially devitalized and cannot transmit the irritation and the pulp 



HYPEREMIA OF THE PULP 391 

recovers its tone gradually. In case nodules or pulp cavity constric- 
tion has occurred, the irritability cannot be reduced in this manner. 
In case of septic dentin this is to be removed and antiseptic substrata 
of filling employed, as above. 

In the indirect cases the cause is removed and the tooth in question 
requires no treatment, except perhaps counterirritation, which is a 
means toward the reduction of any pulp hyperemia. In some cases of 
trauma guards must be applied to adjoining teeth. (See Non-septic 
Pericementitis.) As stated above, certain mild, hyperemic reactions 
after filling require no treatment as a rule. 

Sedatives. — Oil of cloves, eugenol, eugenol and phenol equal parts, 
phenol camphor (equal parts phenol and camphor), thymophen 
(phenol and thymol, p. seq.), menthophenol (menthol 3 phenol 1), 
a saturated solution of thymol in alcohol, a saturated solution of 
menthol in chloroform. 

Solutions of cocain or novocain: Dentalone, Phenandyne and the 
fluid of "jodoformagen" are valuable proprietary agents. To any 
oil, etc., not containing them, menthol, thymol, cocain or novocain 
may be added. 

Oxyeugenol 1 is a sedative temporary filling as is Fletcher's car- 
bolized resin plus zinc oxid. (See page 335.) 

Counterirritation.- — It not infrequently happens that it becomes 
necessary to assist the pulp arteries to recover their tone by means 
of counter irritants applied to the gum over the apex of the root. 
This is especially true in cases of pulp capping. Dental tincture of 
iodin (iodin, 5hj; alcohol, §j; dissolve by succussion; 2 ) or potassium 
iodid, sat. sol., and zinc sulphate, sat. sol., p. seq., with iodin crystals 
to complete saturation 3 is to be applied in spots to the gums, or a 
mixture of equal parts of tincture of iodin and tincture of aconite may 
be painted upon the gum. A mixture made of two parts of tincture of 
aconite and one part of chloroform is recommended by Jack, 4 to be 
applied to the cleansed and dried mucous membrane by means of a 
pad of cottonoid, one-half inch wide by three-quarters of an inch 
long. It should be held in place by the finger for fifteen seconds. 
Tincture of aconite upon cotton, placed in the rubber cup-applicator 
of a cataphoric apparatus and held against the gum for a half minute 
while the current of a few cells is active, will produce a circum- 
scribed area of irritation which may later lose its epidermis. This 



1 Oxyeugenol is composed of Hubbuck's zinc oxide and eugenol in a stiff mixture. 
It hardens in the saliva. The material was introduced by Dr. S. B. Luckie and the 
writer uses the name as convenient. 

2 Flagg. J Northrop. 
4 American Text-book of Operative Dentistry. 



392 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

amount of irritation is valuable. A capsicum plaster may be used. 
For any case of obdurate pain systemic sedation or derivation may 
be employed. (See page 405.) 

The test of success of remedial measures is the gradual reduction 
of response to slight variations in temperature — i. e., the pulp grad- 
ually bears higher and lower temperatures until, approximately, 
a normal tolerance is established. 

As shown by Jack, this varies for hot applications from 118° F. to 
152° F., and for cold ones from 74° F. to 32° F.' 

In order to determine the rate of tolerance normal to the individual, 
he suggests that sound lower incisors be isolated by the rubber dam 
and tested by throwing upon them first water at a temperature of 
80° F. The temperature of the water is then gradually lowered or 
raised until slight pain is produced by the test. The point registered 
by the thermometer will be the normal limit of thermal tolerance for 
the particular test. 

The data gained are useful in determining the progress of a case 
of hyperemia. 

A lack of success in the reduction of the arterial hyperemia is 
evidence that the more severe condition of venous hyperemia has 
supervened, or perhaps an infection has caused a true inflammation. 

When, after fair trial of conservative treatment, the pulp is per- 
sistently irritable, it should be removed. 

In the devitalization of hyperemic pulps there is often painful 
reaction to any of the means employed. Some of these pulps resist 
cocain pressure in any form even after sedation; some yield after 
sedation. Sedation or depletion should precede arsenical applica- 
tions, and if at any time arsenic produce a painful hyperemia or 
aggravate one previously existing, it must be removed and sedatives 
used before its renewal, or it may be applied at another portion of 
the tooth while sedatives are kept against the pulp. Other methods 
of removal are considered in the chapter on Pulp Removal. 

Venous Hyperemia of the Pulp. — Definition. — By venous or passive 
hyperemia of the pulp is meant a condition of the pulp in which 
the return of the blood in the pulp to the heart is mechanically 
prevented. 

Causes, Pathology, and Morbid Anatomy. — But two causes seem 
competent to produce such a venous hyperemia. These are: (1) A 
preexistent arterial hyperemia; (2) thrombosis of vessels at the 
apex of the pulp canal. The venous hyperemia which is the second 
stage of inflammation is to be remembered, but excluded from present 
consideration. It would act by first producing a zone of arterial 
hyperemia which then would produce venous hyperemia. 



HYPEREMIA OF THE PULP 393 

In arterial hyperemia the excess of blood is contained in jnlarged 
capillaries and arterial trunks. The enlarged main trunks or trunk 
at the apex of the pulp must compress the veins, as the apex of the 
canal is unyielding. In proportion to the severity of the arterial 
hyperemia, therefore, are the emergent veins unable to remove the 
blood collected in the capillaries and venules, which gradually enlarge 
into varicosities in consequence (Fig. 359). Black 1 has termed this 
condition infarction an evident misnomer as infarction is due to a 
stoppage of an end artery while venous hyperemia is due to^ stop- 
page of the vein. (See page 27.) 

It has been shown by Hopewell-Smith 2 that thrombosis of the 
small veins and capillaries throughout the pulp may result in rupture 
of the arteries, and hemorrhagic extravasations occur — either single 
or multiple. These he terms hemorrhagic infarcts, although the 
description given more accurately denotes a minute venous hyper- 
emia. (See Fibroid Degeneration of the Pulp.) 

Black has shown that the diapedesis of red corpuscles, which is a 
characteristic result of engorgement of the veins in venous hyper- 
emia, occurs in the pulp. Edema, which usually accompanies venous 
hyperemia in other situations, cannot well occur in the pulp because 
of its unyielding surroundings (Fig. 360) . 

It is possible, however, that fluid may exude into the perivascular 
spaces, compressing the cellular elements. Black has shown that 
deposits of lymph may thus occur in pulpitis. Dewey and Noyes 3 
after carefully conducted experiments upon pulps of dogs and rabbits, 
are of the opinion that lymphatics exist in the pulp so that some of the 
fluid may be thus taken up in partial continued cases. These return 
vessels would, however, be subject to compression like the veins in the 
pulp canal. The intense congestion and distention of the vessel 
walls permit a free diapedesis of red corpuscles into the pulp tissue. 
Disintegration of the red corpuscles may occur and the hemoglobin 
of the corpuscles may be diffused through the dentin, giving it a 
pink discoloration technically known as "suffusion." The infiltrated 
dentin may then become progressively discolored through the 
characteristic changes of color noted in connection with gradually 
decomposing hemoglobin — becoming purplish, dark blue, and finally 
blue black. The color may pass into the yellow or brown coloration 
(see Tomes' case) . Cases have occurred of coronal suffusion in which 
the pulp vitality has persisted for months. In some cases the bulbar 
portion alone may be dead. Thus partial gangrene and the general 
darkening of the tooth may be present even in a single-rooted tooth 

1 Special Dental Pathology, 1915, p. 257. 

2 Dental Cosmos, 1907. 3 Ibid., April, 1917. 



394 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



with the pulp partly alive. This is proof that collateral circulation 
exists in the pulp. In cases of suffusion even all the roots of a molar 
may be suffused, and pericementitis, associated with such a hyperemia 
seems particularly intractable. The vasomotor paralysis is extreme. 
Tomes 1 records a case of a blow upon four upper incisors, which 
became loose and painful. A few days afterward reddish spots 
appeared upon the labial surface, which later became dark blue. 
These disappeared except for a slightly yellowish tint. Four years 
later the pulps were found vital and healthy. This rare case is con- 
firmative of the previous statements. 

Fig. 360 




Section of hyperemic pulp, showing aneurysmal dilatation of the vessels, extra- 
vasations of blood, and red blood disks escaped apparently by diapedesis: a, a, dilated 
vessels; 6, b, b, extra vasated blood. Besides this, red blood disks are plentifully 
distributed everywhere in the neighborhood of the veins. The tooth was extracted 
during a paroxysm of pain. (Black.) 

If a tooth receive a blow of sufficient severity, its pulp may die 
without much evidence of pulp pain. On the other hand, if the 
blow be less severe, it may give evidence of an arterial hyperemia, 
gradually increasing in severity. 



1 Manual of Dental Anatomy. 



HYPEREMIA OF THE PULP 395 

In the former case it is probable that the bruising of the apical 
tissue produces a condition of thrombosis at the apex which involves 
the pulp by shutting off both its arteries and veins. A stagnation 
results, and death from lack of nutrition occurs. This is also termed 
"jugulation." 

In the latter case the thrombosis has not occurred, but an arterial 
hyperemia is set up by the overflow of blood from the apical tissue 
into the pulp, and goes on to venous hyperemia. 

It is quite probable that rapid death of the pulp in pulpitis is due 
to the associated venous hyperemia. 

Kirk 1 mentioned an interesting case of venous hyperemia with 
intense suffusion of all the teeth as the result of hanging. In such a 
case there was arterial blood supplied to the teeth, but the venous 
flow was checked. This is said to be usual. 

Symptoms. — This disease is inferred when the conditions and 
history indicate hyperemia rather than inflammation, and when 
the paroxysms of pain are continuous, instead of temporary — that 
is, when the pain, instead of temporarily subsiding, maintains a 
constant intensity for hours and does not respond promptly to 
sedative therapeusis, and is accompanied by a sense of fulness 
rather than sharp agony. The case from which Fig. 360 was taken 
had been the seat of intense paroxysmal pain for some hours. Upon 
close approach to such a pulp, blueness of the horn instead of 
pinkness may sometimes be seen. It may be noted with light 
transmitted by an electric mouth lamp. 

Prognosis. — Perfect recovery from this condition is extremely 
doubtful, so that if the pulp be not intentionally devitalized and 
removed, it will undergo degenerative changes. The fact that pulps 
have remained alive for years, after having been the seat of marked 
congestion, scarcely warrants the attempt to save so seriously 
crippled an organ. 

Treatment. — The prognosis being doubtful, the pulp should be 
obtunded and devitalized. If the pulp pain does not yield to seda- 
tives, it should be gently exposed if the excavation does not accom- 
plish its exposure. An antiseptic is to be applied, and by means 
of a very sharp puncture probe the pulp is to be delicately punctured. 
A free flow of blood follows, which relieves the vascular engorgement. 
When this is accomplished the cavity is to be syringed out with 
warm water, and a pellet of cotton containing a saturated solution 
of menthol in chloroform may be sealed in the cavity, or simply 
retained by means of a second pellet of cotton saturated with in- 

1 Private communication. 



396 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

spissated tincture of benzoin or chloro-percha. Chloroform alone 
for a few minutes to be followed by an application of eugenol has been 
suggested by Shalit. After twenty-four hours an arsenical application 
may be made for the purpose of pulp devitalization, or the pulp may 
be removed by other means if tolerated. If desired, the bulb of the 
pulp may be taken out under general anesthesia, or the whole pulp 
under mucous or conductive anesthesia or, possibly, under pressure 
anesthesia, though intense hyperemia counteracts, as a rule, (See 
page 312.) 

The extreme paralysis of the vessel walls is occasionally shown by 
persistent hemorrhage after depletion, and which resists ordinary 
effort at limitation. In some cases the intense pain may continue 
as well. The application to the pulp of a mixture of powdered 
thymol and dried alum, equal parts, taken up on a pellet of cotton 
moistened with a saturated solution of thymol in alcohol, or other 
sedative, has proved useful in some cases. A general anodyne may 
be required for relief of the pain. 

INFLAMMATION OF THE PULP (PULPITIS). 

Definition. — Pulpitis is the occurrence of the phenomena of inflam- 
mation within the pulp tissue. The characteristic emigration of 
leukocytes from the bloodvessel into the perivascular tissues must 
have occurred. (See page 37.) 

Causes. — The causes of pulpitis may be classed under three headings: 

1 . Mechanical or physical causes. The pressure of a filling upon a 
thin lamina of dentin or upon an exposed pulp, or even extending 
into it. The pressure of a hemorrhagic extravasation into the pulp 
tissue, the presence of a pulp nodule, or pulp cavity constriction. 
The torsion of a pulp in orthodontia 1 or as a result of trauma as from 
biting hard substances, rapid wedging and mastication upon teeth 
loosened by pyorrhea, the pressure of an impacted tooth upon a 
pulp at the apical region or at a point of resorption are all possible 
causes some of which might also produce arterial hyperemia. In 
cavity cases the force of mastication or suction by the tongue are 
causes while sepsis may be an added cause. 

2. Chemical causes, as oxychlorid of zinc, chlorid of zinc, formalde- 
hyde or other irritant or escharotic used upon the pulp. If any dead 
tissue is formed the effort at exfoliation causes an inflammatory 

1 Buckley, through a circular letter to orthodontists, obtained opinions that the 
upper centrals and laterals are most liable owing to the frequency of displacement, 
character of movement, prominence of location, and the curve of lateral roots. Items 
of Interest, December, 1910 



INFLAMMATION OF THE PULP 397 

reaction on the part of the pulp with intent of exfoliation or absorp- 
tion. 

3. Parasitic or infective causes which cause the phenomena of 
infective inflammation. 

Bacteria may gain access to a pulp in one of five recognized ways: 

(a) Via the dentinal tubules, the fibrils first being devitalized. 
Septic soft dentin under a filling is a cause of this, as is also a sound 
but infected cavity floor. Secondary dentin also may admit infection, 
via its spaces. Goadby has shown that Streptococcus brevis and 
Bacillus necrodentalis may so pass and lately it has been apparently 
proved that apparently hard dentin in vital teeth may contain 
bacteria. 

(b) Via an exposed pulp horn. 

(c) Via a pyorrhea pocket deep enough to admit bacteria to an 
apical space. In single-rooted teeth this may cause rapid death. 
In multirooted teeth a partial pulpitis may occur. The pulp infec- 
tion occurs from the apex toward the crown. Hartzell, observing 150 
cases of sound teeth with dead pulp, suggests (tentatively only) that 
as bacteria were found in some of them the primary cause of death may 
have been infection entering at the gingival margin travelling through 
the pericemental vessels to the pulp. He 1 also has observed strepto- 
cocci in apical regions of teeth, several teeth distant from an abscessed 
tooth. 

(d) Through the extension of an abscess upon an adjoining tooth, 
thus causing an apical infection of the pulp in question and if, of 
rapid extension will destroy the apical tissue and cause pulp death. 
This second pulp may then act as a continuing cause of apical abscess. 

(e) Via the circulation in which the bacteria of influenza or from 
various foci of infection may locate in a tooth pulp. Rosenow 2 experi- 
mented on animals, injecting intravenously streptococci: (1) from 
infected pulp canals; (2) from infected apical tissue; (3) from infected 
tonsils and found it experimentally possible that focal infection 
becoming hematogenous could cause infection of a tooth pulp which 
may explain certain idiopathic hyperemias and inflammations in 
sound teeth or those not offering local explanation. Cases of pulp 
death apparently following influenza have been reported and might 
be due to such an infection from B. influenza existing in the blood. 
As it can produce antral empyemia de now there is no reason why such 
observations should not have credence, if accurate and not merely 
deduced from the presence of devitalized teeth after influenza 
without knowledge of their previous vital character. 

1 Hartzell and Henrici: Journal of National Dental Assn., May, 1917, p. 493, 

2 Journal of National Pental Assn., February, 19 J8, 



398 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



Pulpitis is classified, according to its extent, into partial and com- 
plete; according to its duration, into acute and chronic; according 
to its infective character, into purulent and non-purulent; and, 
again, according to the character of the degeneration which follows 
upon the inflammatory process. While pathologically these con- 
ditions may be clearly differentiated from one another, they may be 
reduced to more compact groupings according to their clinical sig- 
nificance. For example, acute pulpitis is frequently infective, partial, 
and purulent; chronic pulpitis is frequently non-infective, extensive, 
non-purulent, and followed by secondary degenerations. It is, 
however, often purulent, and, of course, infective. 

For the sake of convenience, pulpitis will receive a clinical division 
into acute and chronic. 

Fig. 361 




Inflammation of dental pulp: a, a, normal cells; 6, b, b, b, inflammatory elements: 
c, cells in process of division (yo inch.) (Black.) 



Acute Pulpitis. — By acute pulpitis is meant that form of inflam- 
mation of the pulp which runs an active and more or less violent 
course toward pulp death, and has associated with it, as a rule, 
acute paroxysms of pain. 

Morbid Anatomy and Pathology. — In determining the existence of 
pulpitis, no matter what the symptoms which have presented or the 
condition as to exposure, etc., the microscopic examination of sections 
of the affected organ constitutes the only decisive test; if the changes 
characteristic of inflammation be absent, no matter what the symp- 
toms, pulpitis did not exist. The essential feature of the process is 
emigration of the white blood corpuscles from the small veins into the 
intercellular matrix of the pulp. At first the inflammatory elements 
(leukocytes) are scattered through the spaces between the pulp cells 
(Fig. 361); at a later stage the territory is occupied by round indif- 



INFLAMMATION OF THE PULP 



399 



ferent cells alone. The inflammation may be widespread, as shown 
in Fig. 362, or may be localized to some portion of the pulp, as one 



Fig. 362 




Interstitial pulpitis with pulp nodule in situ. (V. A. Latham.) 

horn of a pulp; Black noted also inflammatory action occurring in 
small islands (Fig. 363). 

Fig. 363 



'^g^^mS^mg^ 



fe?~SSSS3&g 




Minute inflammatory focus within the tissues of the pulp: a, a, arterial twigs; 
b, a nerve bundle; c, collection of leukocytes. (Black.) 



Swelling of the pulp (from exudation) cannot occur unless there be 
a break in the wall of the pulp chamber through which additional 



400 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

space can be gained. Black has recorded that "he found beneath the 
layer of odontoblasts in the region of an exposure an unmistakable 
deposit of inflammatory lymph. The case had a history of severe 
toothache for two days, two weeks previously. The pulp exhibited 
evidences of previous extravasations of blood from hyperemia." 

There is evidence that the pulp may recover from attacks of 
inflammation, and that resolution occurs. In some cases, as shown 
under the head of calcareous degeneration, the tissues may become 
infiltrated with calcic material. In others, chronic degenerative 
changes — inflammatory degeneration — may supervene. 

Suppuration of the pulp is a common accompaniment of pulp 
inflammation; this, being necessarily infective, will be described 
separately. 

Gaskell 1 has reported a case where a central incisor entirely free 
from caries exhibited on its palatal aspect a pinkish tinge, which 
increased in depth until the enamel overlying crushed in, revealing 
the pulp of the tooth lying immediately beneath; there had been a 
resorption of a large mass of the dentin lying between the pulp and 
the enamel. The pulp was removed and the tooth filled. No history 
is given as to the condition of the root, whether resorption had 
occurred there or not. Shortly after, the adjoining central incisor 
exhibited a like pink coloration, which increased, leading to the 
inference that resorption was in progress in this tooth also. At the 
suggestion of E. C. Kirk the patient received continued doses of 
arsenic iodid and the compound syrup of the hypophosphites, in the 
hope of inducing a general and local constructive metamorphosis. 
This treatment was followed by a gradual disappearance of the pink 
coloration, an evidence of a redeposition of dentin. In the absence 
of histological data it is impossible to state just what was the nature 
of the repair tissue in this particular case, but Miller 2 has shown 
that the pulp may take up a resorptive function and remove dentin 
which may later be redeposited as anomalous tissue. The new 
dentin does not contain tubules, but has the characteristics of 
cemental tissue 3 (osteodentin) (Fig. 364). This process has its 
analogue in the tusks of elephants and also in the production of 
Howship's lacunae in the resorption of the pericementum, these 
lacuna? later being filled up with cementum. 

Resorption of the walls of the pulp chamber may occur as an 
accompaniment of chronic pulpitis. What appears to be an idio- 
pathic dentin resorption is described above. Black records a case 

1 Proceedings of the Academy of Stomatology, Philadelphia, 1895. 

2 Dental Cosmos, August, 1901. 

3 Hope well -Smith: Histology and Pathohistology of the Teeth. 



INFLAMMATION OF THE PULP 
Fig. 364 



401 




Resorption of the walls of the pulp chamber and redeposition of new calcific matter : 
a, pulp chamber; b, c, d, portions of resorption areas not refilled and walled off by the 
new deposit-forming cavities occupied originally by the pulp tissue. (Miller.) 



Fig. 365 




Acute pulpitis: ~S, secondary dentin; B, bay-like excavations filled with medullary 
or inflammatory corpuscles; V, transverse section of a bloodvessel; M, multinuclear 
body. X 300. (Bodecker.) 

26 



402 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

where, after pulp capping in a lower molar and the insertion of a 
large gold filling, the tooth was examined at the end of ten years; 
for two or three years the pulp had given evidences of irritability, 
and when the pulp was removed the pulp chamber was found enor- 
mously enlarged and opening into the pericementum between the 
roots of the teeth. Fig. 365 exhibits resorption of previously formed 
secondary dentin with the probable agency through which the 
resorption is brought about. The area of resorption is invaded by 
numerous multinucleated cells, which are evidently performing the 
function of odontoclasts. 

There have been cases of inflamed pulp in teeth decayed while 
yet impacted. In these cases there is usually some form of sinus 
connecting the tooth with the mouth. 

Symptoms. — The early stage of inflammation is an arterial hyper- 
emia, and as the leukocytes collect in the venules a venous hyperemia 
is established. No matter how far the area of stasis extends, beyond 
it will exist an area of arterial hyperemia. Owing to the enclosing 
canal walls and constricted apex a general venous hyperemia may be 
established which causes the death of the pulp. 

In view of these facts it is not surprising that the symptoms of 
pulp inflammation take on somewhat the characteristics of both 
arterial and venous hyperemia. The diapedesis of leukocytes and 
exudation of fluid cause the phenomena of heavy, boring pain and 
a feeling of internal pressure. 

The pulp may be exposed and no symptoms be present. A sudden 
pressure of food or toothpick, suction upon the pulp or the contact 
of cold or hot, salt, sweet, or acid substances, may excite an attack 
of throbbing or lancinating pain. This may be localized in the tooth 
or may be reflected to other teeth or the parts mentioned under 
hyperemia (p. 382). 

The assumption of the recumbent position permits an increased 
flow of blood into the paretic vessels of the pulp and increased 
suffering results in correspondence with the law that inflamed 
parts are always more painful in the dependent position. Indeed, 
recumbency is sufficient at times to induce a paroxysm in a 
comparatively quiet but inflamed pulp. Under a capping or 
filling pressing on the pulp or thin dentin the pain may begin 
as a slight pain and gradually increase in intensity, or it may 
respond as a sudden agony, beginning even some time after the 
operation. This may have been known at the time of operation or 
been suspected later. In one typical case, violent reflexes occurred 
sometime after a metal filling was introduced over sound dentin. 
The diagnosis was uncertain but filling removal and placement of 



INFLAMMATION OF THE PULP 403 

oxyeugenol cement for a month, removed the reflexes, permanent 
filling was done and after four years no trouble exists — diagnosis, 
pressure irritation. In the later stage of pulp inflammation the 
pain is of a heavy, boring, continuous character, the pericementum 
becomes somewhat hyperemic (see Fig. 354), and the tooth responds 
to tapping. In case of a highly irritable pulp, however, the concussion 
of the pulp produced by tapping may readily cause pain. 

In pulpitis the pulp responds both to heat and cold. There have 
been many cases of reflex neuroses developed by inflamed pulps, 
reflex pains in the face, eye, ear, neck, scalp, chest, arm, heart, etc., 
as well as functional disorders of the eye, ear, and brain; a large 
number of facial neuralgias are due to this condition whether the 
pulp be intact or partially destroyed as in pulp abscess or ulceration. 
(See Neuralgia.) One case of dementia prsecox was cured by removal 
of a tooth with inflamed exposed pulp. 1 Kauffmann 2 cites a case of 
aphasia with hallucinations cured by removal of an inflamed pulp. 
One case of sensory paralysis of the entire left side was caused by 
inflammation of a portion of the pulp in a right upper cuspid and 
marked relief began in about an hour after removal of a covering 
dressing and filling. The symptoms of suppurative inflammation 
may differ somewhat. (See Abscess and Ulceration, p. 406). 

Diagnosis. — The diagnosis is largely inferential and made by 
observation of the symptoms and conditions existing. The pulp 
may be exposed or closely approached by caries, or the pulp may 
be approximated by a large filling. If there be a leak about the 
filling, a septic fluid or actual decay beneath the filling may be the 
exciting cause. In the absence of evident causes such sepsis is always 
to have consideration, and, if necessary, the filling must be removed 
and tests applied. The more obscure causes, such as abscesses upon 
adjoining teeth, infection from the pericemental tract in the course 
of pyorrhea, looseness of teeth or traumatisms, are to be carefully 
considered. If the tooth involved be uncertain, each tooth should 
be placed under rubber dam and tested thoroughly. The conditions 
are either obvious causes of pulpitis or if obscure those indicating 
hyperemia are to be carefully considered first. Ordinarily practical 
exposure indicates pulpitis at least for clinical purposes while non- 
exposure either at the horn or apex leads to inference of hyperemia to 
be further tested by consideration of the causes (see page 381), and 
probably by treatment as for hyperemia. If this is not successful 



1 Upson: Dental Cosmos, 1910, p. 529. 

2 Dental Cosmos, November, 1916. 



404 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

a presumption of profound venous hyperemia or inflammation exists. 
The pulp must be removed in either of the latter two conditions. 

Prognosis. — The prognosis is always bad for the comfortable 
conservation of the pulp, and it should be removed and the canal filled. 

Treatment. — The treatment of pulpitis involves the reduction of 
the amount of blood in the vessels of the pulp, the sterilization 
of the infected area, the relief from the pain, and the removal of 
the pulp. It is usual to excavate the cavity of decay thoroughly 
enough to remove from over the pulp decayed dentin which would 
prevent the action of remedies or act as an irritant. The cavity is 
then washed and a sedative applied. (See p. 391.) A creamy paste 
of bicarbonate of soda in carbolic acid has been recommended. The 
use of chloroform as a first application to be followed by eugenol 
when the pain ceases has been recommended by Shalet. 1 The addi- 
tion of a trifle of powdered alum to any of the sedatives acts as an 
astringent to the vessels. During the half hour succeeding the 
application the pulp should give some indication of relief. If it 
be somewhat decided, a portion of the remedy used should, if pos- 
sible, be sealed in the cavity for twenty-four hours. The covering 
may be prepared first as for arsenic (q. v.). If not possible to 
to seal it in, it may be covered with cotton saturated with a varnish 
made by evaporating tincture of benzoin. This varnish hardens 
like sandarac varnish, but, unlike it, is not irritant. Claims are 
made for alcohol used as for pressure anesthesia. 

If after the first half hour no indication of relief has been obtained, 
it is well to expose the pulp and to relieve the engorged vessels by 
delicately puncturing it. (See Extirpation of Pulp.) After exposing 
the pulp it will perhaps exude a bead of pus, which makes the diag- 
nosis one of pulp suppuration. After free bleeding, which may be 
encouraged by means of warm water, the sedatives will usually act. 
It may be necessary at times to employ short general anesthesia 
(nitrous oxid gas, etc.) as a means to obtain free bloodletting. Every- 
thing being prepared, the patient is anesthetized and the bulb of the 
pulp cut out, or if N 2 and O anesthesia can be used, the entire pulp 
may be taken out. Conductive anesthesia may be used. At times 
cocain pressure anesthesia is effective at least for the removal of the 
bulb of the inflamed pulp, and sometimes of the entire pulp; often, 
however, it causes too much pain. When several trials have been 
made, and even the cotton forced into the pulp tissue without com- 
plete anesthesia, a pellet of arsenical devitalizing fiber may be put 
into the pulp chamber with no discomfort as a rule. 

1 Dental Digest, March, 1917. 



INFLAMMATION OF THE PULP 405 

In case of partial extirpation, not only is free bleeding induced, 
but the diseased pulp tissue is largely removed. When hemorrhage 
• ceases arsenic may be applied, or pressure anesthesia attempted. 
If the hemorrhage be obstinate the application of powdered thymol 
and dried alum may be used. (See Venous Hyperemia.) When 
sedatives are used upon the pulp, counterirritants applied to the 
gum are aids of great value, and are to be used as described under 
Arterial Hyperemia (p. 391). 

In addition to these the principle of depletion may be employed. 
Deep cuts may be made with a sharp bistoury in the gum overlying 
the root apex. The anastomosis with the vessels of the apical tissue 
is expected to cause the cuts to act as openings made in veins leading 
from the inflamed pulp. According to Nancrede, depletion on the 
venous side of an inflamed area markedly reduces engorgement. In 
addition to these measures catharsis is a valuable means of derivation ; 
a tablespoonful of sulphate of magnesia is to be dissolved in a goblet 
of water and taken internally at least a half hour before a meal. 

If the pain be obdurate and its return feared, two | grain sulphate 
of morphin tablets may be dispensed, preferably by the operator, 
to be taken only in case of severe pain and an hour apart. 
Acetanilid and phenacetin, aspirin, trigemin and bromural, 5 grains 
each, repeated if necessary, are also useful. 

The following is a useful anodyne and antineuralgic prescription: 

]$ — Acetphenetidini (phenacetin) , 

Acetanilidi ...... '. ...... aa gr. xxx 

Quininae sulphatis gr. xv — M. 

Pone in capsulas no. vi. 

S. — One morning and evening. 

(See also Treatment of Facial Neuralgia.) 

Hall 1 has suggested : 

1$ — Aspirin 3ss 

Codein gr. iss 

M. et. ft. chart. No. vi. 

Sig. — One every half- hour until relieved. 

Quiet of the pulp must be secured before an arsenical application 
is made, or the latter merely increases the irritation instead of 
promptly devitalizing (an exception is noted above). Should such 
an irritation occur or be feared, arsenic may be sealed in an opening 
made in another part of the tooth (a "pocket" 2 ), with a view to 
devitalizing the pulp through an avenue of healthy pulp tissue. At 
the same time the pulp may be quieted b} r sedative applications 
made in the cavity of decay. 

Instead of drilling a special pit, the arsenic may be applied at a 

1 Dental Cosmos, 1910, p. 1085. 2 Flagg. 



406 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



portion of healthy dentin in the cavity, which is at some distance 
from the orifice of exposure; over the latter the analgesic may be 
placed arsenic pentoxid has been suggested by Fette as being 
sedative (see Pulp Removal). 

SUPPURATION OF THE PULP. 



Fig. 366 



Definition. — By suppuration of the dental pulp is meant a forma- 
tion of pus on its surface (ulceration) or in its substance (abscess). 
It occurs both as an acute and as a chronic affection. 

Causes. — The immediate cause of suppuration of the pulp is the 
ingress of pyogenic organisms to the pulp. As in inflammation of 

the pulp, while usually associated with 
direct exposure of the pulp, suppuration 
may occur in pulps covered by softened 
or even unsoftened dentin. 

Arkovy 1 first observed infection of 
the pulp while still covered by a layer 
of unsoftened dentin (Fig. 366) . 

Goadby has shown that microorgan- 
isms may penetrate even secondary 
dentin, a condition not infrequently 
seen. Miller states that sections of 
the overlying dentin in a case of sup- 
puration of the pulp showed the same 
forms of bacteria as were found in the 
pulp itself. If we follow Hartzell and 
Henrici 2 in the belief that streptococci (brevis, viridans) are the 
primary agents of pulp infection and staphylococci secondary agents, 
we must conclude that staphylococci are the agents of the suppur- 
ation. 

Bacteria which have entered the body through wounds, etc., may 
be deposited in the pulp as well as in any other part of the body, 
wherever there may be a lessened resistance at the time. While 
bacteria may thus enter from the circulation, there is usually abun- 
dant opportunity for their entrance from the mouth. Suppuration 
of the pulp is a not infrequent sequel of the capping of pulps which 
have given evidence of a previous hyperemia or inflammation. 

Morbid Anatomy and Pathology. — Anatomically pulp suppuration 
(purulent or pyogenic pulpitis) is of two general varieties: one begins 
upon or close to the suface of an exposed pulp, and gradually destroys 




Invasion of pulp by micrococci. 
(Arkovy.) 



1 Diagnostik der Zahnkrankheiten. 

2 Journal of National Dental Assn., May, 1917, p. 487. 



SUPPURATION OF THE PULP 



407 



the organ through a process of progressive ulceration (Fig. 367); 
the second, that confined in the substance of the pulp, causes the 
gradual destruction of a part of the pulp through the formation of 
circumscribed abscesses (Fig. 368). 

Ulceration of the Pulp. — Of these two forms, ulceration is the 
more common. The capillaries (Fig. 367) are blocked with coagu- 
lated blood (they are left open in the illustration to clearly mark 
their position); the intercapillary meshwork is occupied by inflam- 

Fig. 367 




A, diagram of lower molar with caries at a which exposes the pulp; the darkened 
portion at b shows the extent of the inflammation; the rest of the organ was free from 
inflammatory change. B, illustration of the inflamed tissue, showing a part destroyed 
by suppuration at a; the odontoblasts are undermined at b; the bloodvessels which 
were filled with blood clot in the section are left blank here, that they may be more 
apparent. (Black.) 



matory exudation ; the surface of the pulp is eroded and covered with 
pus corpuscles; the ulcerative process is undermining the layer of 
odontoblasts. The suppurative process penetrates the body of the 
pulp, following the direction of its veins and hollowing out the organ 
into a deep cavern. Black regards the persistence of the layer of 
odontoblasts as indicating an inferior vitality, as it shows they are 
less susceptible of change of form than the other cells of the organ. 
The process of ulceration may continue for weeks or months until 



408 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

the entire organ has been destroyed molecularly. The necrotic por- 
tions undergo putrefactive decomposition, probably passing through 
the same stages that any albuminous substance passes in its serial 

Fig. 368 




Acute suppurative pulpitis in the coronal portion; I, intensely inflamed horn; A, 
abscess; V, bloodvessels engorged with blood; *S, superficially inflamed horn; N, nest 
of inflammation. X 10. (Bodecker.) 



decomposition, into the end-products — ammonia, carbon dioxid, 
hydrogen sulphid, and water. 

I have observed cases of vital but finally ulcerated pulps under 



SUPPURATION OF THE PULP 409 

canal fillings. In one case twelve years had elasped between the 
partial canal filling and the more recent observation. In another 
case in which temporary stopping had been packed upon vital 
filaments fifteen years passed before I opened and found them. 
There were no symptoms and I supposed the tooth devitalized 
because the pulp cavity appeared to be filled (Fig. 369). 

Symptoms. — If the cavity of decay be open the pus and serous 
exudate may freely escape, so that the symptoms may not exceed a 
dull, gnawing pain, which is usually re- 
flex in character. Fig. 369 

As a rule, the response to cold will be 
much delayed or even absent. Intense 
pain may exist when the pus cannot 
find exit owing to food debris being 
massed in the pulp chamber, or owing 
to the presence of a filling or mass of 
secondary dentin. The case then re- 
sembles and practically becomes one of 



■HflB 



abscess <rf the pulp. ^ Crowned lower molar with pulp 

The chief diagnostic feature of pulp filaments vital for fifteen years. 

ulceration is the presence of the sub- 
acute inflammatory symptoms described above and the presence 
of a pulp partially removed by decomposition of its upper portion. 

Thus if the pulp chamber be open at one horn, and a probe may 
be passed into it for a short distance until it comes into contact with 
an irritable portion of pulp, and when withdrawn have the odor of 
putrefaction, the diagnosis is clear — loss of pulp substance by putre- 
factive changes, presumably by suppuration. In some teeth it may 
be by partial gangrene. Many phases of this condition may be seen; 
thus in an extreme case one canal of a lower molar contained a highly 
irritable vital filament of pulp extending but one-quarter inch from 
the apical foramen; a second canal was entirely occupied by a per- 
fectly vital but ulcerating filament; the third canal contained an 
entirely dead pulp. The bulb of the pulp had disappeared, doubtless 
by suppuration. 

Treatment. — The treatment of pulp ulceration in its early stages 
involves the opening of the orifice of exposure, the sterilization of 
the superfices of the pulp, and pulp removal. 

Superficial sterilization may be accomplished by removing the 
pus or putrefactive material present by means of warm 3 per cent, 
hydrogen dioxid. The saturated solutions of thymol in alcohol or 
menthol in chloroform, or 2 per cent, formaldehyd or formocresol 
diluted to 3 per cent, formaldehyd strength with eugenol may be 



410 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

sealed in position against the pulp for twenty-four hours as an anti- 
septic. I have even used pure formocresol in the pulp chamber with- 
out irritation, sometimes erroneously having diagnosed putrefactive 
pulp, but later the vital filaments were discovered. The application 
of arsenic may then be safely made. In favorable cases the bulb of 
the pulp, or even the entire pulp, may be removed at the first or second 
sitting by means of cautiously applied cocain and phenol pressure 
anesthesia. In some cases, however, the patient will rebel. 

When a part of the canal filament alone remains after treatment 
to remove bacteria, the pressure anesthesia may be resorted to. A 
long thread of cotton is saturated with carbolic acid or carbolic acid 
and cocain, and gently packed into the canal against the pulp fila- 
ment. Pressure with vulcanizable rubber is now produced, and after 
a few minutes the pulp will be sterilized and anesthetized sufficiently 
for removal. It is better to treat each canal separately as a general 
pressure will probably fail. Puncturing is also useful at times. 
Arsenic may be cautiously placed on cotton half-way up a canal 
against such a pulp filament. Another method consists of packing 
a thread of cotton dipped in carbolic acid tightly against the fila- 
ment, in which thrombosis is thus induced. (See also Methods of 
Pulp Removal.) 

Abscess of the Pulp. — Abscess of the pulp is usually situated near 
the point of exposure of the organ. It may be confined to one horn 
of the pulp, or may involve nearly the entire substance of the pulp, 
the peripheral tissue of the pulp being unbroken. Abscess may exist 
at some distance beneath the surface of the pulp, and the latter be 
still covered with a layer of dentin. Burchard once uncovered the 
horn of a molar pulp which was covered by a lamina of hard dentin, 
and no fluid appeared ; but upon passing a sharp probe into the white 
area of exposure for over one-eighth of an inch or more there was a 
free flow of pus which quickly filled the larger carious cavity. A pulp 
removed entire from a tooth, and which was yellowish white in color 
and unbroken, showed upon section its interior hollowed out into an 
enormous abscess cavity (Fig. 370). The bloodvessels were blocked; 
the peripheral tissues were unaltered; between the odontoblasts and 
the abscess cavity, the latter lined with pus corpuscles, evidences of 
inflammation were plenty. In some cases pus flows upon removing 
a last layer of dentin, a pulp capping, filling, etc. While technically 
this is ulceration, being superficial, yet a cavity is circumscribed and 
contains pus so that the condition and symptoms are those of abscess 
of the pulp. Black found that the odontoblasts retained their form 
after neighboring cells of the pulp had been destroyed. 



SUPPURATION OF THE PULP 



411 



Miller's 1 researches show a preponderance of cocci and micrococci 
in cases of enclosed abscess; cocci and diplococci were of constant 
occurrence. Many of the forms, both cocci and bacilli, were cultivable 
upon gelatin and agar-agar,. Some of them, cocci and bacilli, brought 
about the liquefaction of gelatin; others did not. So that it must be 
inferred that infective inflammation and necrosis of the pulp may 
occur without suppuration. (See Gangrene of the Pulp.) In some 
instances streptococci were found. In the freely exposed pulps 
varieties of organisms were found which would render clear the 
possibility of a general infection by way of the dental pulp. 

Fig. 370 




Transverse section of inferior bicuspid pulp, one-half diagrammatic: a, abscess 
cavity; b, embryonic cells at the periphery of the abscess cavity; c, occluded blood- 
vessels. (Burchard.) 



Symptoms. — The usual symptoms are as follows: In a tooth con- 
taining an enormous filling, one in which the pulp has been exposed, 
or nearly so, or in a tooth having a large carious cavity, the patient 
gives a history of discomfort or decided pain, appearing at intervals, 
sometimes appearing and disappearing suddenly, the existing condi- 
tion having been ushered in by dull, gnawing pain, which is usually 
not positively located, although it may be. The pain grows in 
intensity, and, in contradistinction to the pulp conditions previously 
described, pain is relieved instead of increased by applications of cold. 
It may be, however, that the prolonged contact of iced water may 
induce a response. The response to heat is marked, so that a mouth- 

1 Dental Cosmos, 1894. 



412 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



Fig. 371 




ful of hot coffee or even the warmth of the tongue may precipitate an 
attack of severe and continued pain. Pain produced upon passing 
from a warm to a cold atmosphere, and vice versa, is also symptomatic. 
If the pulp be freely exposed and pricked with a sharp instrument, a 
flow of pus follows in many cases, and the relief is almost immediate. 
In the earlier stages a period of throbbing pain may follow evacu- 
ation of the pus. In some cases a very minute portion of odorous 
liquid may be found at a very fine exposure. 

In other cases the response to 
heat may decrease until it is almost 
absent, and the case only be seen 
when evidences of the action of 
bacterial products upon the peri- 
cementum appear, which they 
usually do in the later stages of 
pulp suppuration, when the tooth 
becomes loose, extruded, and tender 
upon percussion. 

The symptoms of pericemental 
disturbance may simulate those of 
incipient, acute, apical abscess, 
even though a quarter of an inch or 
more of apical pulp tissue exist 
in a vital though highly inflamed 
condition. Upon clinical evidence it is assumed that the inflammation 
of the pulp produces inflammation of the apical tissue, or that the 
infection travels to the apical tissue (Fig. 371.) In one case the gum 
and contiguous parts about an upper molar were swollen, apical 
abscess diagnosticated, and a free flow of pus followed by blood 
obtained upon opening the crown. An examination made twenty- 
four hours later, after symptoms had subsided, demonstrated all 
three pulp filaments to be alive when a post hoc diagnosis of extensive 
abscess of the pulp was made. If untreated, symptoms of pulp and 
pericemental disturbance may disappear for weeks or months; but 
if the parts be not perfectly sterilized and reinfection prevented, it 
is only a question of time when septic pericementitis will arise. 

Diagnosis. — The most valuable diagnostic symptoms are (1) the 
peculiar increasing reaction to applications of heat and relief from 
cold; (2) the sudden appearance and disappearance of the pain — 
often while in the office; (3) the response to change of atmosphere, all 
of which are confirmed by opening and finding; (a) a bead of pus on 
the pulp surface; (6) a fine insensitive horn evidently putrefactive with 
vitality beneath as it is explored; (c) pus upon puncturing the pulp. 



Abscess of the pulp after forma- 
tion of a large amount of secondary 
dentin, dividing the pulp into two 
portions: S D, secondary dentin; A P, 
abscess or confined pus; V P, vital 
pulp; /, area of apical inflammation. 
(Diagrammatic.) (After case in the 
mouth.) 



SUPPURATION OF THE PULP 



413 



In cases where several teeth are involved in the diagnosis, differ- 
entiation is made by isolation of each tooth by means of a small 
square of rubber dam. The thermal test is then applied. The pres- 



Fig. 372 




Chronic suppurative pulpitis terminating in calcification of the pus and atrophy of 
the pulp: A 1 , larger abscess, filled with calcified pus; A 2 , abscess at the periphery of 
the pulp ; A 3 , A 3 , small longitudinal abscesses, all calcified ; N, calcified nerve bundle ; 
C, C, calcareous depositions in the fibrous pulp tissue; P, P, pigment clusters from 
previous hemorrhage. X 10. (Bodecker.) 



ence of a quantity of secondary dentin will confuse by causing dulness 
of response. In such case the electric test should be resorted to. 
It may fail if much pus be present in which case the electric light 



414 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

should show opacity. (See Dry Gangrene.) In some cases secondary 
dentin will have formed in the pulp cavity and the abscess may be 
found in one of the filaments, while the other will be apparently 
healthy. Fig. 371 is a diagram of a number of cases seen in practice. 
It is to be remembered that the expansion of the gas by heat with 
symptoms of pain is common to all cases with gas confined, whether 
a pure pulp abscess, a partial gangrene (putrefactive) or even total 
gangrene with apical irritability. Therefore one should be prepared 
to modify the tentative diagnosis according to the condition found 
on investigation after opening, which is always warranted. 

Prognosis. — General experience regards ulceration and abscess of 
the pulp as precursors of the death of the organ. Usually this is 
by progressive suppuration. It is undoubtedly true, however, that 
attempts at circumvallation of the dead tissue are made in some 
cases (Fig. 371). The pus cells undergo degeneration and the abscess 
site may be the seat of calcareous deposits. Even in these cases 
death is delayed, not averted.* The remainder of the pulp under- 
goes atrophic changes, and commonly suppuration reappears. 

Treatment. — The treatment of the case consists in relieving the 
existing pain, completing the devitalization of the pulp, and removing 
it in such a manner that no organisms or dead matter are carried 
beyond the apex of the root. 

To secure relief, evacuation of the pus is imperatively necessary. 
The organ is freely exposed, exercising no pressure in gaining free 
access to it. If pus does not flow upon exposure of the surface of 
the pulp, a sharp, slender, sterilized probe is quickly passed into the 
substance of the pulp, when, if pus be present, it will usually escape 
freely through the opening thus made and be followed by blood. 

Throbbing pain may follow, which a sedative promptly quiets. 
The application is not made until the pus flow ceases. One of the 
sedatives mentioned for ulceration (page 409) is laid upon the pulp 
and the cavity is sealed for twenty-four hours (never longer), and 
then the pulp is removed. Should the exposed portion of the pulp be 
insensitive it is cut away until access is had to the vital portion, 
where the arsenic is to be applied. The pulp may sometimes be 
anesthetized by cocain for removal. The rubber dam need not 
necessarily be applied for the treatment preliminary to devitalization, 
but the pulp should be kept under the influence of antiseptics. As 
these may be obstinate cases the pulp may be removed surgically or 
at least the bulb may be removed, using anesthesia as described on 
pages 312, etc.) 



CHRONIC INFLAMMATION OF THE PULP 415 

CHRONIC INFLAMMATION OF THE PULP. 

In cases in which the resistive force of the pulp is great and the 
causes of less violent nature or less violent in action, the inflammation 
may be of low grade and continue for some time. Pulp ulceration 
may pursue a chronic course, as has already been described. Abscess 
of the pulp may also become chronic, and the pulp may even encap- 
sule the pus area, and, the bacteria dying, the abscess area may 
become the seat of calcareous deposits. 

Fig. 373 




Chronic inflammation of the pulp, areolation, and degeneration (Black.) 

Sclerosis of the Pulp. — Inflammation of a low grade may persist 
in the pulp for long periods, giving rise to an increase of its fibrous 
tissue with atrophy of the cellular elements, producing a condition 
found in chronic interstitial inflammation in some other tissues — a 
sclerosis. Instead of the usual distribution of myxomatous tissue, 
bands and bundles of fibrous tissue appear. The pulp appears 
shrunken and stiff, bloodvessels are contracted and sclerotic, and 
the nerve fibers have undergone partial or complete atrophy and 
degeneration (Fig. 373). 

Black found that in the late stages of sclerotic atrophy areolae 
developed in the bundles of connective tissue, the inflammatory 
elements having disappeared and the areola? being occupied by 
fluid. Arkovy describes the condition as reticular atrophy of the 
pulp. 

Sclerotic and other chronic degenerations of the pulp usually 
present the history of one or more attacks of pulpitis in the past, 
with more or less continuous uneasiness extending over a long period. 
The response of the pulp to all tests becomes diminished and dull. 
The condition cannot be diagnosed before pulp removal. 

Treatment. — Such pulps are to be devitalized and removed. 

Chronic Hyperplastic (Hypertrophic) Pulpitis. — When the pulp 
is exposed over a wide area, long-continued chronic inflammation 



■416 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



may lead to an enlargement of the organ with a protrusion of an 
altered pulp mass through the orifice of exposure, producing the 
condition known clinically as fungous pulp. When the growth 
extends beyond the boundaries of the orifice and then increases in 
bulk it forms a pedunculated mass to which the term polypus of the 
pulp has been applied. 

Fig. 374 




Pulpitis arteriosclerosis; nerve degeneration. (V. A. Latham.) 



Morbid Anatomy and Pathology. — The growth has its origin in a 
chronic inflammation of the body of the pulp; the organ swells, and 
contact with the sharp edges of the orifice of exposure excites a 
continued irritation, leading to further proliferation of the cells of 
the inflamed part, so that a large mass of embryonic tissue is formed 
(Fig. 375), termed by Black granulation tissue of a low type. As in 
the granulation tissue of repair, bloodvessels grow into this mass, 
so that it may bleed at a slight touch. Black noted in his case illus- 
trated, a covering of squamous epithelium upon the periphery of the 
growth, which might be interpreted as the transformation of meso- 
blastic into epiblastic tissue, but the correct explanation beyond 
doubt is that advanced by the same author, that the epithelium is 
transplanted from the gums, and grows after the manner of a skin 
graft. The growth does not contain nerves. The cavity in which it 
lies is often fairly free from decalcified dentin, the walls appearing as 



CHRONIC INFLAMMATION OF THE PULP 



±Y1 



though subjected to an absorbent action. Black ascribes this to the 
action of saprophytic bacteria upon the decalcified dentin, but other 
chronically inflamed hyperplastic pulps have absorbent action (see 
page 400) and there is no good reason to make this an exception, 
though of course there is no means of proof. 

Fig. 375 




A, a first lower molar with a cavity at a completely filled by an hypertrophy of the 
pulp, which has grown out through the orifice, exposing the pulp at b. B, a field 
illustrating the tissue of the growth, which is composed almost entirely of granulation 
tissue of a very primitive type; a, a covering of epithelium presenting papillae; b, 
epithelium apparently without papillae. (Black.) 

These growths may undergo further changes; higher organization 
of the granulation tissue occurs and fibrous tissue is formed ; the cells 
may undergo degenerations, first granular, then fatty, and suppura- 
tion and gangrene may occur. Tomes 1 records a case where calci- 
fication of an hypertrophied section of a pulp occurred; but as the 
case was due to traumatism (fracture of a tooth), different vital 
conditions existed from those in the cases under discussion. (See page 
361.) Actual calcification of the mass is scarcely possible, although 
calcareous degeneration may occur within the fungous mass (Fig. 
376, 6r). These tissues seem to have an inherent vitality peculiar to 



27 



Dental Surgery, third edition. 



418 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



the patient. I have seen cases of separated portions of pulp all vital 
with one hypertrophic or with one hypertrophic and the other dead. 



Fig. 376 



M— 




Hyperplastic myxomatous pulp, which filled a carious cavity: M, lobules made up 
of papillse of a myxomatous structure, rich in capillary and venous bloodvessels; G, 
calcareous globule; E, epithelial cover of papillse. X 10. (Bodecker.) 



Fig. 377 



Fig. 378 



Fig. 379 



Fig. 380 



"Br~fr 




Hypertrophy of pulps. (Garretson.) 

As shown by Miller, Hopewell-Smith, and others, a reconstructive 
change may occur and adventitious dentin be redeposited in the 
area of resorption (Fig. 364). 



CHRONIC INFLAMMATION OF THE PULP 419 

Symptoms. — The symptoms of chronic pulp inflammations and 
degenerations are usually those of long-continued discomfort, with 
reflex pains, which rarely persist into the latest stages of degeneration. 
The response to heat and cold, present at first, declines until the 
pulp scarcely reacts, and then but slowly. 

No nerve fibers develop in the hypertrophic pulp tissue, so that 
the newgrowth has no sensitivity in itself, although pressure upon it 
may cause sharp pain through the still vital pulp nerves themselves. 

Four or five of these hypertrophies may exist in a mouth, filling 
whole cavities of decay, the surrounding tooth structure being in 
various stages of disintegration. They seem to be comparatively 
insensitive to mastication (Fig. 378). 

Fig. 381 Fig. 382 




Hypertrophy of the gum. Hypertrophy of the pericementum. 

(Garretson.) (Garretson.) 

Hypertrophy of the pulp also may be associated with pulp ulcera- 
tion, the growth arising from one canal of a tooth. 

Regeneration of an extirpated pulp has been claimed. These are 
probably referable to the above form of hypertrophy, or to a fungoid 
growth from the pericementum or supposed extirpation under cocain. 

Diagnosis. — The only condition with which hypertrophic pulp may 
be confounded is a pedunculated growth of gum tissue through a 
cavity at the neck of a tooth beneath the gum margin, or through 
a perforation either accidental or by caries (Fig. 382). It is impor- 
tant to differentiate between these conditions, because, if an appli- 
cation of arsenical paste be made to a fungous gum, the destruction 
of tissue may extend into the sound pericementum. The physical 
appearances of the two are alike; they both bleed freely and have 
about the same degree of sensitivity. 

Histological examination of this class of hypertrophy of the gums, 
conducted by Dr. Luigi Ancone, 1 of Italy, demonstrated that the 
growth is a simple exaggeration of the normal elements of the part. 
Occasionally a sarcomatous growth arises in this region, i. e., from 
the marginal pericemental tract and if not self-explainable as, for 

1 Abstract from l'Odontologia, by Dr. W. Dunn, in International Dental Journal, 1899, 



420 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

example, in Fig. 382, and not rapidly amenable to treatment calls 
for a resection of a portion of the bone. 

If the tumor be central to the tooth tissue and the latter not 
decayed out to very thin walls, it may be at times laid aside by means 
of a blunt instrument and be seen to have its origin from an orifice of 
exposure (Fig. 377). As a rule, a hyperplastic pericementum will 
be found to have its attachment much lower or more lateral than 
a hyperplastic pulp, and the pulp cavity be seen to have been enlarged 
by caries, even more than shown in Fig. 300. It is then fairly inferred 
to be a gum mass, especially if the tooth has never been operated 
upon. The diagnosis may be a doubtful one, in which case the 
rubber dam is to be applied, the polypus frozen by means of a spray 
of ethyl or methyl chlorid, and the mass removed with a sharp 
blade passed across its peduncle. The electric cautery may preferably 
be used to ablate the mass. Local anesthesia may be used in con- 
junction to eliminate pain or even for removal of the pulp. 

The source of the tumor may then be usually clearly seen. As an 
alternative proceeding the tissue may be thoroughly saturated with a 
strong solution of trichloracetic acid and then ablated. If any fur- 
ther doubt exist, the pulp is to be sterilized with hydrogen dioxid, etc., 
and a pellet of cotton saturated with oil of cloves, carbolic acid, or 
dental tincture of iodin is laid upon it, and over this temporary stop- 
ping is firmly packed, or cotton and sandarac first dipped in ortho- 
form may be used. By this means the growth may be pressed away 
until it is seen to arise from either a pulp chamber or a perforation 
made by decay or accidental excavation into the pericemental tract. 

Radiography should aid in the diagnosis. Hemorrhage may be 
checked with alum and thymol in powder or solution, or by the use 
of trichloracetic acid, silver nitrate, zinc chlorid, or iodin. 

Treatment.— If the case be one of pulp hypertrophy, arsenic may 
be applied or local anesthesia attempted for pulp removal. 

Crystals of iodin have been used with satisfaction in combination 
with pressure for pulp devitalization. 1 If a perforation exist, it is to 
be treated by sealing the orifice with gutta-percha, copper amalgam, 
or oxyphosphate of copper cement. (See page 300.) 

Infarction of the Pulp. — The production of infarction may result 
(see page 393), and as described consists of minute circumscribed 
hemorrhages from end arteries into the pulp tissue. This differs 
somewhat from a true infarction (Fig. 383). It cannot be diagnosed. 

Fibroid Degeneration of the Pulp. — Apart from the degenerations 
due to inflammatory conditions, a form of degeneration occurs "as a 

1 Pr. James Truman. 



CHRONIC INFLAMMATION OF THE PULP 



421 



natural old-age termination of the life of a healthy pulp, and similar 
to senile changes occurring in the pericementum." (See Fibroid 
Degeneration of Pericementum). This change, as described by 
Hopewell-Smith, 1 occurs in teeth of the aged in whose mouths simple 
alveolar resorption has occurred, though later he 2 has shown that it 



Fig. 383 




H, hemorrhagic infarct; R, rupture of bloodvessel; D, dent/n; O, vacuolated odonto- 
blasts; F, early fibrosis of pulp. X 250. (Hopewell-Smith.) 

may occur in the pulps of young persons, in sound teeth extracted 
for irregularity, and even in teeth in which the dentinal wall or pulp 
cavity is not completed to a typical calcification. He regards it 
as due to a primary thrombosis of the capillaries and veins, with 
permanent dilatation of the arteries, with or without tiny hemor- 
rhages, the lack of collateral circulation and lymphatics con- 



Histology and Pathohistology of the Teeth. 



2 Dental Cosmos, 1907. 



422 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



tributing to the atrophy. As a cause he suggests chemical change 
in the blood through systemic derangement, as anemia, chlorosis, 



Fig. 384 




Horizontal section of fibroid degeneration of the pulp in situ. Prepared by Mr. 
Hopewell-Smith's process: D, deeply stained dentin; S, large areolar spaces; DO, 
degenerate odontoblasts; P, fibroid tissue of pulp. X 45. (Hopewell-Smith.) 



or exhaustive diseases, the red corpuscles being fewer and the 
leukocytes and blood platelets increased, thus favoring a thrombosis 
of small vessels; also, that here inflammatory changes in the peri- 



CHROMIC INFLAMMATION OF THE PULP 



423 



cemental tissue might interfere with the pulp circulation sufficiently 
to produce it. 

Clinical Significance. — While the form of thrombosis or fibrosis 
may not be diagnosed because of lack of related symptoms, 
Hopewell-Smith argues that they should be suspected in weak and 
unhealthy patients, and that such suspicion should contra-indicate 
conservative operations, also that they may explain certain difficulties 
of devitalization or anesthetization of the pulp or cause a related 
change in the pericementum or brittleness in the dentin. 

Fig. 385 




Fibroid degeneration of the pulp: D, dentin with tubules; FO, fibroid odontoblasts; 
P, atrophied pulp tissue. 



Morbid Anatomy. — "The odontoblasts become sheaved with or 
without fatty degeneration; the arteries, permanently distended, 
undergo hyaline degeneration; a reticular atrophy occurs, with dis- 
appearance of cells and nuclei of both pulp and vessels and nerves, 
and, at the same time, the connective-tissue fibres undergo hyper- 
plasia. The pulp goes more or less gradually through the stages 
shown in Fig. 383, finally producing the stage shown in Figs. 384 
and 385, in which the pulps are shrunken and may have left the wall 
of the pulp chamber. "Many areolar spaces appear which may be 



424 



DESTRUCTIVE DISEASES OF THE DENTAL PULP 



arranged in chains. The odontoblasts are degenerated. The pulp 
stroma is very dense, has a clear, fibrous structure, becomes very 
marked in staining, and is highly differentiated from the surrounding 
tissue. The bloodvessels, nerves, cells, and connective-tissue have 
all disappeared, and their place is taken by a new, firm, fibrous 
structure devoid of cells, nuclei, or any regular arrangement of 
constituent parts." 

Fig. 386 




Fatty degeneration of the pulp. (V. A. Latham.) 



"There is no calcification of the pulp and no obliteration of the 
dentinal tubules. 

"The proximate cause and associate phenomena are not as yet 
clearly related." 

Fatty Degeneration of the Pulp. — During the course of degenera- 
tion of the elements of the pulp fatty changes may occur as in other 
parts. The fatty changes occur in the walls of the arteries and 
sheaths of the nerves, and in the odontoblasts. (Hopewell-Smith.) 

Cloudy swelling also appears. (Latham.) (See Figs. 386 and 387.) 



CHRONIC INFLAMMATION OF THE PULP 425 

Fig. 387 




Cloudy swelling; parenchymatous degeneration; pulp nodules. (V. A. Latham. 1 ) 

Fig. 388 




Colloid degeneration of the pulp. Compare with Fig. 29. (V. A. Latham.) 

1 Dr. Vida A. Latham's illustrations are from her paper on Some Pathological 
Features of the Pulp, Journal of the American Medical Association, September 22, 
1906. 



426 DESTRUCTIVE DISEASES OF THE DENTAL PULP 

Fig. 389 




Great thickening of nerve bundle. From a case of chronic neuralgia. Patient had 
many teeth extracted for neuritis. (V. A. Latham.) 



Fig. 390 




Neoplasm of the pulp. (V. A. Latham.) 



CHRONIC INFLAMMATION OF THE PULP 421 

Colloid Degeneration of the Pulp. — The demonstration of colloid 
material within the pulp has been made by Latham, as shown in 
Fig. 388. She states that it may become calcified. The condition 
is very rare. Other degenerations such as Wallerian, hyaline, and 
amyloid have been noted. 1 It would seem that the pulp may be 
subject to any form of degeneration seen elsewhere. 

Nerve-end Degeneration of the Pulp. — The degeneration of nerves 
occurs in the pulp as it may in the pericementum and from the 
same causes that produce endarteritis. The bundles may be enlarged . 
Neuralgia may be associated with it. 

Neoplasm of the Pulp. — Latham claims that a neoplasm may occur 
in the pulp, and offers the photomicrograph shown in Fig. 390 as 
proof of the fact. I do not know of any cases in which such a pulp 
condition has been related with a malignant growth outside of the 
pulp cavity, though it may not be impossible. 

Many of the destructive pulp diseases occur in the pulps of the 
temporary teeth, and are to be treated in like manner, except as to 
the use of arsenic, which, being accompanied by greater danger, 
should, for the most part, be replaced by other methods of pulp 
removal. This point is discussed at length in the chapter upon 
Removal of the Pulp. 

If the tooth roots be largely resorbed, the pulp may bear capping 
even when ulceration has occurred. The pulp may die under this 
capping, when the case is further treated as indicated. (See Chronic 
Apical Abscess.) 

1 Talbot: Dental Cosmos, 1909, p. 1150. 



CHAPTER XIV. 

METHODS OF REMOVAL OF THE DENTAL PULP 
AND ROOT-CANAL FILLING. 

The removal of the dental pulp is predicated upon subsequent 
root filling. If not done, an apical abscess probably will later result. 
As all root fillings are at present scientifically shown unreliable the 
considerations here presented are tentative and in anticipation of 
the hoped for discovery of better methods. There are four general 
methods by which a patient or pulp may be prepared for the opera- 
tion of pulp extirpation. These are as follows: 

1. Anesthetization of the patient and removal of the pulp during 
the period of anesthesia. 

2. Anesthetization of the apical tissue by mucous local anesthesia 
or of a main nerve branch (conductive anesthesia) and the removal 
of the pulp. 

3. Anesthetization of the pulp by cocain or novocain (procain), or 
in some cases by nervocidin, or by freezing and the removal of the 
pulp. 

4. Devitalization of the pulp followed by its removal. 

1. General Anesthesia. — The pulp of a single-rooted tooth may be 
readily extirpated while the patient is anesthetized by nitrous oxid, 
nitrous oxid and oxygen, or by somnoform. The instruments should 
be in readiness, the patient anesthetized, the pulp uncovered by 
an engine bur, and the pulp extirpated with a barbed broach or 
Donaldson cleanser. 

In cases of multirooted teeth the available anesthetics are ether, 
which is rarely used for the purpose, and nitrous oxid and oxygen 
administered by nasal inhalation; a true anesthesia is required as 
distinguished from analgesia described on page 312. 

The ordinary nitrous oxid outfit is, however, of value by enabling 
the operator to remove the diseased bulb of the pulp of a multirooted 
tooth, after which and while the patient is conscious other methods 
of removal of the radicular portions of the pulp may be employed. 
(See page 404.) 

2. Anesthesia of the Conductive Apparatus. — The second general 
principle consists in the use of mucous, diploic or conductive anes- 
thesia to block the transmission through the fifth nerve leading from 

(428) 



ANESTHESIA OF THE PULP 429 

the part. This has been previously described for hypersensitive 
dentin (see page 314). Sometimes in conductive anesthesia it fails 
for the pulp while other tissues seem anesthetized (Blum) or the apical 
portion of the pulp may be sensitive (Reithmiiller) a condition difficult 
of explanation, except on the ground that some nerve tracts or fila- 
ments are not affected. Otherwise the pulp may be painlessly 
removed. The success of mucous and diploic anesthesia depends 
upon infiltration of the apical tissue. These methods are Aery valu- 
able in all cases of difficulty with diseased pulps and indeed are choice 
methods in any pulp removal. The objections are that extirpation 
may not be complete owing to the insensitivity, or that one may even 
operate on apical tissue, producing pericementitis. The use of phenol 
may obviate the first difficulty. Claims have been made for a slight 
sidewise blow struck upon the tooth to paralyze the pulp nerves by a 
stretching shock. 

3. Anesthesia of the Pulp. — For this purpose cocain hydrochlorid 
or novocain are generally employed. There are three practical 
methods by which it may be introduced into a pulp: 

Pressure Anesthesia. — By pressure accomplished by means of raw 
vulcanite. A strong solution (50 per cent, to saturated solution) of 
cocain hydrochlorid or novocain is made in water, or preferably in 
some mild antiseptic solution which does not cloud on admixture (as 
Borine) in order to avoid infection of pulp or apical tissue. A small 
piece of amadou (spunk) or cotton is saturated with it and laid upon 
the orifice of exposure. The cavity is filled with the rubber, a flat 
strip being fed first into the cervix and later folded into the cavity. 
This confines the solution better, and upon this is placed a flat-ended 
plugger or burnisher broad enough to concentrate the force upon the 
cotton. A broad piece of cotton placed over the rubber is sometimes 
of assistance in preventing slipping. Gentle pressure is now made 
and a slight pain is usually felt. The pressure should be maintained 
until this passes away, then it is increased little by little until some 
force is exerted. The rubber and cotton are then removed, the pulp 
cavity opened, the progress of the anesthesia tested with a fine broach 
and the pulp lifted away. Some prefer to place a prepared billet of 
cocain or novocain upon the pulp, others prefer chloroform, eugenol or 
alcohol as the solvent. Novocain is understood as equal to cocain. 

For multirooted teeth the pressure should be prolonged, and to 
prevent return of sensation and hemorrhage while extirpating it is 
well to instil carbolic acid into the pulp tissue by means of a fine, 
smooth broach. - 

In some cases the operation fails because the direction of the 
pressure has been away from the pulp or because the cotton has 



430 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

slipped from its place. Sometimes the orifice of exposure may be 
enlarged, but as sensation is discovered a fresh application must be 
made. In cases with large foramina the application may fail; with 
the incomplete foramen of moderate size it is more successful. 

Sometimes repeated applications fail to effect, though the appli- 
cation is not painful, and at times the pressure is not tolerated at 
all, owing to the irritability of the pulp, due to continued hyperemia 
or inflammation. Even six or eight applications have at times 
failed even when a fair and accessible exposure existed. Sedation 
for a day or two sometimes permits a successful application. This 
action of cocain corresponds to that in inflamed tissue. Sometimes, 
even when the cotton enters the pulp tissue, the pulp is still sensitive 
higher up. In such a case I have often packed devitalizing fiber 
into the pulp in place of the cotton and without further pain. In 
cases of cavities without walls to confine the rubber, it is well to 
enclose the buccal and lingual embrasures with the thumb and 
forefinger. In very broad occlusal cavities the finger-tip confines 
the rubber nicely. 

When only canal filaments are present, any septic matter present 
should be removed by syringing repeatedly with an antiseptic solu- 
tion, or better formocresol 1 part, eugenol 5 to 7 parts applied for a 
day or two; then the canals should be thoroughly dried, and the cocain 
dissolved in an antiseptic, is carried on a cotton thread into the canals 
and against the pulp remnant. A small piece of rubber is placed in 
one canal and the pressure confined to that canal by means of a 
plugger which will about fill the canal. The action is then repeated 
in the other canals. This produces better results than a general 
pressure over all the canals at once. 

If used after arsenic has been applied the results are not usually so 
good, but sometimes the method is successful. To avoid the intro- 
duction of arsenic into apical tissue all sloughing portions should be 
removed and all arsenic washed out. 

When the pulp is not exposed, the application to the dentin over 
the pulp permits advance, a pocket being created in the dentin with 
a bur, which aids the further instillation of the cocain; finally, the 
pulp is exposed and the anesthesia is completed. 

Clyde Davis recommends for the purpose of producing the exposure 
the use of a drop of 1 to 1000 adrenalin chlorid followed by a drop of 
37 per cent, formaldehyd, then pressure with raw vulcanite. 

Where calcific formations are present they present some difficulty, 
though with persistence one may be enabled to anesthetize the pulp. 
Custer recommends 75° to 90° sulphuric acid to aid in loosening 
the nodule. Cook recommended an application of 10 per cent. 



ANESTHESIA OF THE PULP 431 

sulphuric acid for a few minutes, followed by sodium bicarbonate 
previous to a reapplication of the pressure anesthesia, as highly 
effective in aiding penetration of the cocain. Desiccation is always 
a valuable preliminary, aiding penetration. Claims are made for 
eucain, or alcohol for producing pulp anesthesia by pressure. 

There is a possibility of the introduction of cocain into the general 
circulation, and some systemic effect may be noted, though often 
this will be due to the agitation of the patient. Some patients have 
complained of tingling in the fingers. If syncope be threatened 
aromatic spirit of ammonia should be administered, the head lowered, 
the feet elevated, and smelling salts or amyl nitrite applied to the 
nostrils. It is always well to administer aromatic spirit of ammonia 
or camphorated validol before using cocain for any purpose. In some 
cases of fracture exposing the pulp a crystal of cocain laid against 
the pulp has caused anesthesia by mere absorption; if this fails it will 
at least prepare for pressure anesthesia. 

Hemorrhage following the extirpation of the pulp is sometimes 
copious. To avoid this, carbolic acid should be instilled into the 
pulp tissue by means of a smooth broach. A fine Donaldson cleanser 
may be passed to the apex of the canal and slowly twisted, the oper- 
ation consuming several minutes. This torsion of the pulp largely 
limits the hemorrhage. If it occur it should be allowed to check 
itself, though if desired a trifle of a mixture of powdered alum and 
powdered thymol may be taken upon cotton wet with phenol- 
camphor and passed to the end of the canal. Deliquesced zinc chlorid 
checks hemorrhage promptly; a dilution is less painful. 

It is an open question whether canals from which living pulps 
have been removed should be filled immediately or not. There is 
liable to be a secondary hemorrhage, particularly when adrenalin 
is used with the cocain. Many prefer to fill at once, claiming that 
surgical pericementitis is the only result. Ottolengui has suggested 
the use of dry cotton to absorb any blood. If this is bichloridized or 
otherwise antisepticized it is better. The writer as a rule places phenol 
camphor plus menthol on cotton as a sedative antiseptic. This, as a 
rule, permits the healing of the parts without much tenderness, and 
really consumes but little more time in the aggregate. It seems best 
to avoid formaldehyd in this connection, though the writer in this 
yields to the general sentiment rather than from much fear of modified 
formocresol. Still there is nothing gained by irritating normal tissue. 

High Pressure Anesthesia. — When considerable dentin overlies the 
pulp, or when a tooth is sound, the most expeditious method of pulp 
anesthesia is the introduction of a 2 per cent, solution of cocain or 
novocain by means of the compound syringe. This consists of a 



432 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

strong metal syringe, the piston of which is actuated by means of 
levers which multiply the power of the hand. The Myers syringe is 
one of the best, though several forms are obtainable (see Fig. 322). 
The syringe nozzle is embedded in a small hole drilled in the dentin by 
one of two methods : The hole may be made small with parallel sides, 
as when drilled with a No. \ bur; the syringe nozzle has then slightly 
conical sides at the point, intended to jam a fit when introduced with 
force into the drill pit. In the other method the drill pit is made 
with a cone-pointed bur or bud bur, and the syringe point is made 
flat-ended, a form easy to maintain upon the point. All air must 
be expelled from the syringe. It is wise also to expel all air from 
the drill pit by a slight pressure while the syringe point is loosely 
held in the pit. Then a rotary motion under forward pressure 
embeds the point. 

If no leakage occurs the force of the piston drives the anesthetic 
through the fibrils in the tubules and into the pulp. The pressure 
must be maintained for about three minutes, though several applica- 
tions may be made each time drilling into the point of sensation. The 
anesthesia is then tested by drilling with a No. \ bur in the direction 
of the pulp. If the dentin be sensitive the syringe is to be reapplied. 
Often the bur sinks into a sensitive pulp without warning by dentinal 
sensitivity. In such case the syringe is reapplied for a moment, when, 
as a rule, the anesthesia will be complete. In all cases when testing 
the drill hole should not be enlarged, as this prevents reapplication. 
Too much cocain should not be introduced, as it has happened that 
the area about the apical tissue has been profoundly injected, with, 
of course, possibility of systemic complication. This warning 
applies to the second application rather than the first. Novocain is 
less dangerous. When desirable, the enamel of a sound tooth which is 
to be crowned may be ground away until the dentin is reached, or 
if enamel must be removed in only limited degree, as for a tap upon 
the lingual side of an incisor or in the fissure of a bicuspid, a "spot" 
is first made with a dentate bur, then a spear drill is driven through 
the enamel only just reaching the dentin. The drill hole is then 
enlarged as widely as permissible, after which the pit is made in the 
dentin with a No. \ bur. 

The lingual side of upper incisors will permit of sufficiently direct 
pressure to enable the operator to center the syringe point, but in 
many cases in which crowns are indicated the labial side may be 
used with advantage, especially at the neck when the cementum is 
exposed. Later, the entrance tap is made in line with the pulp axis 
and the first opening closed with cement (finally with silicate if crown- 
ing is not intended). The occlusal surfaces or parts of cavities may 



ANESTHESIA OF THE PULP 433 

be used in upper posterior teeth. The labial or mesiobuccal side must 
always be used in the lower teeth, unless a cavity be used, sometimes 
preferably at the neck, sometimes higher up. In cavities having suffi- 
cient dentin over the pulp the pit may be made in the pulpal wall, and 
if for any reason it is needed the drill pit may begin at the cervical 
portion of the cavity and extended into the root dentin and parallel 
with the pulp. The pit must be deeper than the syringe point will 
penetrate, so that the pressure may force the solution laterally through 
the tubules, which are at a right angle to the axis of the pulp and the 
pit. There are occasional failures with this method. I recall a lower 
molar sound but the pulp hyperemic. Drilling, at first intended to 
reach the dentin only, was carried to the pulp without pain. Anes- 
thesia was begun with confidence but abandoned after an hour of 
trials including ordinary pressure anesthesia. Arsenic was completely 
successful. In some cases solutions of antiseptics have been as effec- 
tive with this instrument as the cocain solution. The experiment 
may not be successful. 

According to Brouardel, 1 of Paris, the effects of cocain are acute 
and chronic. The former develop usually in ten or fifteen minutes, 
or even up to three-quarters of an hour after the injection. They are : 
precordial anxiety, filiform and extra rapid pulse, lividity of the face, 
coldness in the extremities, and abundant perspiration; rise in tem- 
perature, irregular respiration, tingling sensations in the hands, 
blunted tactile sensibility, excitement, loquacity, weeping, anger or 
hysterical fits; bilious vomiting with or without diarrhea, anuria, 
symptomatic epilepsy, followed by motor and sensory paralysis. 
Death occurs in from two minutes to five hours after administration, 
though in the chronic cases fatality usually does not result. 

Placing the patient in the horizontal position, giving inhalations 
of amyl nitrite, and, if further cardiac stimulation be necessary, hypo- 
dermic injections of ether or strychnin are indicated. Strong coffee is 
to be administered before dismissal in any untoward case and giving 
30 minims of aromatic spirit of ammonia or 6 drops of camphorated 
validol in a little water previous to operation is a wise precaution even 
with novocain. 

The chronic poisoning occurs mostly in those addicted to its use. 
Some develop a tolerance of the drug, withstanding from 30 to 120 
grains. Tachycardia and intense psychic disturbances, leading to 
physical and mental collapse, are observed. 

Cataphoresis. — The third and least desirable form of cocain anes- 
thesia of the pulp consists of its introduction by 4 the cataphoric cur- 

1 Dental Cosmos, 1905, p. 150S. 
28 



434 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

rent. (An ionization apparatus is similar and can be used, see p. 327.) 
It has the disadvantage of consuming more time, but may serve when 
patients are timid. A 10 per cent, solution of cocain hydrochlorid 
is applied to the pulpal wall of the cavity, the tooth being previously 
placed under rubber dam. The anode of the cataphoric outfit is 
applied to the cotton and the cathode placed in the hand or at the 
cheek. 

The dentin may be anesthetized as well; fifteen minutes or more 
may be required to get an exposure. If desired, this method may be 
used to obtain a pulp exposure and the pressure method employed to 
complete the operation. 

When beginning with an exposed pulp, about fifteen minutes will 
be required unless hyperemia of the pulp exists, when a longer time 
will be needed. As with the pressure method, there may be occa- 
sional failures. It will be noted that there is advantage in time and 
convenience in the pressure and blocking methods. 

Carbolic Acid. — The fourth method of producing pressure anes- 
thesia consists in the use of carbolic acid in place of the cocain, or in 
case of obstinate canal filaments of a solution of cocain in carbolic 
acid on cotton packed against the pulp filaments. The method is as 
in ordinary pressure anesthesia. While an anesthetic it probably 
acts by devitalizing protoplasm through coagulation of albumin. 
(See p. 410.) 

Nervocidin. — The fifth method of producing pulpal anesthesia is 
by the application of nervocidin, an alkaloid obtained by D. Dalma 
from the East Indian plant gasu-basu. Arkovy recommended that a 
portion be applied to the exposed pulp for twenty-four hours, when 
it may be removed painlessly. Soderberg 1 suggests the addition of 
a small amount of cocain hydrochlorid to overcome the primary 
irritating effect of the nervocidin. If dentin be over the pulp, an 
additional application of twenty-four hours' duration is required to 
obtain an exposure. (See p. 326.) 

Freezing. — Sprays of rapidly vaporizable substances, such as ethyl 
or methyl chlorid, directed against the exposed pulp, the tooth being 
isolated under rubber dam, will, in some cases, render the pulp entirely 
insensitive, although, as a rule, they fail to entirely anesthetize to 
the apical foramen. Ice is formed which acts as a non-conductor. 
The method is painful and not applicable in many cases of highly 
irritable pulps. (See p. 325.) Ottolengui has suggested several 
applications of ether on cotton to slowly refrigerate the pulp bulb 
and finally leaving the cotton while the first spraying with ethyl 
chlorid is done. 

1 Dontal Cosmos, 1901 and 1902. 



DEVITALIZATION OF THE PULP 435 

4. Devitalization of the Pulp. — Devitalization of the pulp by the 
use of arsenic trioxid as a preliminary to its successful removal 
is the oldest of the methods employed at the present day, 1 and 
as shown, it still has to be resorted to either from necessity or 
convenience. 

The method has its value in the very teeth in which its use is least 
objectionable, namely, the posterior teeth. There is no danger of 
the use of arsenic in teeth having completed roots, or in unresorbed 
temporary teeth, provided the arsenic be accurately sealed in the 
cavity so that it does not escape upon the gum. If it does escape it 
may destroy the gum or pericementum and cause partial necrosis of 
bone or the complete loss of the tooth together with some bone. The 
pulp always dies through a process of venous hyperemia induced by 
the protoplasmic irritant and poison. Some of this is absorbed by 
the pulp. This hyperemia is progressive from the pulp bulb toward 
the apex of the root, and there it causes the death of the apical portion 
of pulp through interference with its nutrition. Sometimes this 
hyperemia of the pulp extends into the apical tissue, but if the pulp 
be left in situ, necrosis of apical tissue never results, but, on the 
contrary, the hyperemia becomes resolved after the death of the 
pulp. 

The writer fails to see wherein such a hyperemia differs in conse- 
quence from that produced by the surgical removal of a pulp and 
denominated with favor as surgical pericementitis. In his hands 
such teeth have given quite as good results as when other methods 
have been employed. By this it is not meant that there has been 
no difficulty in devitalizing some pulps, particularly some of those 
in which repeated applications of cocain under pressure failed to 
anesthetize, but that when carefully handled and sufficient time for 
pulp death has been allowed, careful filling of the canal has been 
successful. 

There have been assertions made that a condition favoring apical 
granuloma results from the use of arsenic, but when the collateral 
lack of asepsis, leaving of pulp tissue, poor root filling, etc., is taken 
into consideration, this is not a result proved against the arsenic. 
Indeed the indictment against all root fillings as not mechanically 
perfect may explain this result. (See page 467.) 

Action of Arsenic upon the Pulp. — Arkovy 2 was the first to point 
out the details of the action of arsenic upon the dental tissues : 

"1. As 2 3 brought into contact with the tooth pulp acts in the 
following way : A certain degree of inflammatory hyperemia, total or 

1 Introduced by Spooner in 1836. 

2 Transactions of the International Medical Congress, London, 1881. 



436 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

partial, depending upon the quantity of the agent applied, sets in; 
the bloodvessels become expanded, and here have a tendency to 
thrombosis. This latter effect may also be in connection with 
embolism of the capillaries, when the agent is quickly taken up into 
the bloodvessels. 

"2. AS2O3 produces no coagulation of tissue whatever. 

"3. It has a specific influence upon the blood corpuscles, combining 
with the hemoglobin to form a compound of arsen-hemoglobin, and 
of this chemical process there seems to be evidence in the profuse 
yellowish tinge of the whole pulp tissue and in the discoloration of 
blood in several of the bloodvessels. 

"4. In nearly every case it is taken up in substantia (in form of 
molecules) into the blood- ways; when there it produces besides the 
above-mentioned changes, granular detritus of the contents and 
anemic collapse — shrinkage, the latter effect being brought about 
nearly exclusively in cases where greater doses were used. 

"5. The bulk of the pulp tissue — viz., connective-tissue fibers and 
odontoblasts — undergoes no change whatever; not so the connective 
tissue cells, which increase three or four times their normal size. 

"6. The special action of arsenic trioxid upon the nerve element 
consists in the following: the neurilemma is only so far influenced 
that its nuclei are somewhat increased; a more essential change takes 
place in the axial part, where, after the application of more than 
1 mg., granular destruction of myelin sets in, and the axis-cylinder 
commences here and there to disappear. A very surprising alteration 
may be seen in the notchy tumefaction of the axis-cylinder, described 
heretofore almost only in cases of central lesions. 

" 7. All these alterations occur in and among normal-looking tissue. 

"8. The action of arsenic trioxid is macroscopically exhibited by 
a brownish-red tinging of the whole or of certain parts of the pulp 
body, as well as of the neighboring dentin and the cementum, this 
latter in cases treated with greater doses — viz., 2 to 5 mg. This 
alteration is most expressed at the top of the crown pulp and at 
the apical one-fourth to one-third part. This circumstance may 
be considered as an external evidence of the devitalization being 
completely attained to." 

Miller's experiments 1 upon the tails of mice (made without and 
with rings at the root of the tail to simulate the surrounding of the 
apical vessels of a tooth; made without and with encasement of the 
tails in plaster of Paris to imitate the rigid surroundings of the dental 
pulp) showed that in the absence of the plaster encasement enormous 

1 Dental Cosmos, 1894. 



DEVITALIZATION OF THE PULP 437 

edema of the tail was produced and a sensory paralysis of the hind 
limbs; complete anesthesia of the tail occurred in forty-eight hours. 
" The action of arsenic appeared somewhat accelerated when a glass 
ring was applied close to the root of the tail. In more than forty cases 
there was not one in which the action of the arsenic extended beyond 
the ring, and the action was not appreciably affected by enclosing the 
tails in plaster casts. The action of the arsenic is of a progressive 
nature, beginning at the point of application and extending gradually 
in each direction." 

Flagg 1 devitalized ten pulps and removed them, cut off the portion 
of the bulb of each which had contact with the arsenic, and tested the 
ten pulps together by Reinsch's test. Arsenic was found, estimated 
at a one-hundred-thousandth part of a grain, or one-millionth of a 
grain for each pulp. Prinz has later confirmed this. Allowing for 
possible mechanical introduction or contact of arsenic during extirpa- 
tion, the quantity of arsenic introduced by the circulation must be 
very minute indeed. 

Flagg argued that as the pulp subsequently putrefies it cannot 
have died as the result of arsenical poisoning alone. 

In the roots with large foramina arsenic may be absorbed, as areas 
of devitalization of the apical and overlying gum tissue have been 
noted. In several apparently authentic cases the pericementum of 
a mature tooth has been said to be destroyed from the apex down 
and the tooth lost. I have never seen such a case resulting from the 
arsenical method alone in either clinical or private practice, although 
cases of marginal gum, alveolar, and pericemental death, beginning 
as the result of leakage or application to perforations, have been 
noted. It is probable that as stasis proceeds the apical portion of 
the pulp becomes involved in advance of arsenic absorption. Miller's 
experiments show that arsenic does not pass the point of constriction. 

Variations in the Action of Arsenic. — In most cases of fully formed, 
single-rooted teeth in young adults an application of arsenical paste 
directly to the exposed pulp will be followed by the complete death 
of the organ in forty-eight hours. At the expiration of that time a 
sterilized broach may be passed almost to the apex of the root and 
the pulp removed en masse without pain. Pulps of molars require a 
longer time, often a week, before the filaments are dead. The finer 
filaments resist longer than the larger ones. If pulp nodules exist, 
the action of the arsenic may be delayed or in some cases be almost 
nil. In calcareous and other chronic pulp degenerations the action 
is also delayed. If arsenical applications are made over a layer of 

> Dental Cosmos, 1868. 




43S REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

dentin, the same delay is noted, and is increased in very dense 
teeth. There is also a greater tendency to suffusion. 

Some pulp, irrespective of the pulp condition, exhibits a peculiar 
idiosyncrasy in resisting the action of arsenic, requiring large doses 
and long applications before succumbing. Second applications often 
require more time to kill the balance of the pulp than the first appli- 
cation would have required. The time used in investigation is 
practically lost. The editor, therefore, allows plenty of time; about 
ten days for molars, five for single-rooted teeth, and prefers to find 
the pulp entirely dead. 

The rational objections to arsenic, aside from its escape upon the 
gum, are: (1) The possible production of pain. (2) Possible suffu- 
sion of the tooth. (3) The time required. 

The production of pain may largely be obviated by observance of 
certain technique. The pulp should ordinarily be exposed and be 
slightly bled to relieve any hyperemia or inflammatory engorgement 
present, as this seems to prevent the absorption of the arsenic. A 
powerful sedative, such as thymol, menthol, cocain hydrochlorid 
or morphin acetate, should be employed as a corrective, and the 
menstruum should be sedative rather than coagulant. All pressure 
on the pulp should be avoided as this produces pain. 

Prinz has suggested the rational improvement of using a con- 
centrated solution of cocain or novocain before applying arsenic. 
This renders its primary action less painful or painless. 1 This is 
practically done when one obtains a partial anesthesia only when 
pressure anesthesia is tried and abandoned for arsenic (see p. 430). 

Sufficient time for complete death should be allowed. If, 
upon examination with a fine smooth broach, vitality be dis- 
covered, a sedative should be applied and pulp death awaited. 
Leaving the dead portion against the vital part of the pulp is 
even better than making a second application, as its removal re- 
lieves the congestion by opening the vessels, and the congestion is 
necessary to the end in view. If the pulp give but little response 
upon probing it may be removed. Plunging a bur into the pulp 
cavity sometimes produces a slight pain probably referable to impact 
upon liquid pressure being felt at the apex as there may be no further 
pain. In some cases a still vital filament is the explanation. Some- 
times the diapedesis of red corpuscles, associated with the venous 
hyperemia, causes a staining of the pulp and dentinal fibrils with the 
liberated hemoglobin (see p. 393). This is unfortunate, but can be 
treated by bleaching with 25 per cent, ethereal pyrozone sealed in 

1 Dental Materia Medica and Therapeutics. 



DEVITALIZATION OF THE PULP 439 

the pulp cavity for about twenty-four hours after the pulp is removed 
and the canal partly filled. The third objection, the matter of time, 
does not apply to the cases of prompt devitalization, as the time spent 
in pulpal anesthesia and checking hemorrhage is in the aggregate no 
less than in the arsenical cases. In the delayed action of arsenic the 
objection is valid, but the mucous, diploic, conductive and general 
anesthesia methods are still open to trial. The arsenical method, of 
course, requires a longer waiting period. Pulpal anesthesia can be 
tried when arsenic does not act well, but should be avoided when it 
originally failed. It is not apt to succeed. As stated, these considera- 
tions apply mainly to posterior teeth. 

Forms in Which Used. — The following is an excellent formula for 
arsenical paste: 

1$ — Arsenici trioxidi gr. xv 

Cocainse hydrochloridi gr. xx 

Thymolis (vel mentholis) gr. v 

Olei caryophylli q. s. ft. pasta — M. 

This should be finely ground in a mortar and spread over the bottom of a wide glass 
jar so that some of the paste may be taken up from the bottom. The arsenic settles 
to the bottom. 

Buckley recommends the following formula: 

1$ — Arsenic trioxid . gr. clxxx 

Cocain alkaloid gr. xxx 

Thymol gr. xv 

Petronal TUxv — M. 

Either of the above may have the powdered ingredients mixed. 
The cotton pellet may be wet with the menstruum and then dipped 
into the powder. Lamp black added to the paste colors it so that it 
is easily distinguishable in a cavity. (Buckley.) 

The following are other formulae: The analgesics included are 
intended to dilute the arsenic and quiet the pulp, and thus both 
directly and indirectly modify the pain. 

1$ — Acidi arsenosi, 

Morphinae sulph aa gr. x 

Acidi carbolici • q. s. ft. pasta — M . 

(J. D. White.) 

1$ — Acidi arsenosi gr. x 

Morphinae acetatis gr. xx 

Olei caryophylli q. s. ft. pasta — M. 

(J. Foster Flagg.) 
Creosote may be substituted for oil of cloves or phenol. 

]$ — Acidi arsenosi gr. x 

Cocainae hydroch. . . . • gr. xx 

Olei cinnamomi q. s. ft. pasta — M 

(E. C. Kirk.) 

1$ — Arsenic gr. x 

Alum gr. x 

Thymol gr. x 

Oil of cloves q. s. ft. pasta — M. 



440 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

As the ordinary pastes tend to separate into layers of arsenic, 
morphin, etc., and menstruum if made thin, they should either be 
made into stiff pastes or spread over the bottom of a wide jar, so that 
some arsenic may be scraped off the bottom at each application. 

W. H. Truman indorses the opinion of J. D. White that 
thorough trituration for two hours more finely divides the arsenic 
and prevents separation, and claims that the use of arsenic 
triturated with wood creosote and glycerin is the most effective 
preparation. 1 

Miller offers the following general rules as deductions from his 
observations : 

"1. The rapidity and intensity of the action of arsenous acid 
depend, under certain circumstances, to a very considerable degree 
upon the substance or substances with which it is incorporated. 

"2. Where there is but a small point of exposure, and in particular 
where extensive calcification has taken place in the pulp, escharotics 
should be avoided, since the coagulation of the tissue retards the 
absorption of the arsenic. This retardation is but slight where there 
is a broad surface of exposure. In stubborn cases, where applica- 
tions of the ordinary paste fail to effect the devitalization, a paste 
consisting of arsenous acid in oil of cloves, glycerin, or salt solution 
should be employed, undiluted by any third constituent. 

"3. Thymol is worthy of a trial as a substitute for morphin, on 
account of its anesthetic and antiseptic properties. 

"4. For devitalizing pulps of temporary teeth or remains of pulp 
tissue in root canals, arsenous acid, if employed at all, should be 
diluted with two or three parts of some other constituent (thymol, 
zinc, oxid, morphin, iodoform)." 

Cobalt was introduced by Robert Arthur as a devitalizing agent 
some forty years ago. Within recent years it has been employed, 
notably by the Herbst method, to destroy pulps. The cobalt paste 
of Herbst was analyzed by E. C. Kirk, and found to consist of 
metallic arsenic and cocain hydrochloride Kirk suggests that free 
acids which cocain salts may contain, or the chlorin from the chlorid, 
may combine with the metallic arsenic and form soluble salts. The 
use of arsenic pentoxid and soluble arsenates has been suggested by 
Fette, and for which he claims advantages. 2 

Fette 3 recommends the use of arsenic pentoxid formed into a paste 
with glycerin as applicable upon inflamed pulps as even at times 
relieving pain and ordinarily not causing any. 



1 Dental Brief, June, 1913. 2 Dental Cosmos, November, 1914. 

3 Ibid., p. 1240. 



DEVITALIZATION OF THE PULP 441 

Brun 1 strongly recommends chemically pure cobalt and cocain 
hydrochlorid equal parts plus carbolic acid as having satisfactory 
devitalizating action, not passing the foramen, not causing gum 
necrosis and even acting through dentinal fibers. 

His variants are: (1) with formocresol for purulent pulpitis; (2) 
with sodium hydrate 10 per cent, in children's teeth; (3) to avoid pain 
applying without excavation and repeating the next day after excava- 
tion; (4) with mucous anesthetic injection applied to pulp stumps 
after removal of the bulb only. In this case on a ball of cotton, 
wet with phenol and dipped into cobalt powder. A week or more is 
required for devitalization. The covering preferred is zinc oxid and 
eugenol into which cotton is incorporated at the time of mixing; on 
account of discoloration the method is confined to molars. 

There are some advantages in the so-called devitalizing fiber intro- 
duced by J. Foster Flagg. To make this, absorbent cotton is cross-cut 
with scissors to a fine lint or short fibers. This is dusted into the paste 
or ground up with it in the mortar. It may then be dried on a blotter 
and be bottled for use. As it lacks long fibers, a small portion may be 
detached and be placed upon the pulp. There are cases, however, 
in which the paste should be carried to the exposure upon a probe 
and gently inducted into a fine exposure. Here its tendency to spread 
or penetrate is valuable. The fiber has no such tendency, which 
makes it less dangerous in use. In making the application a minute 
portion of paste is to be laid upon the pulp, or a pin-head pellet of 
cotton is rolled in it, the excess of menstruum removed, and it is 
then applied to the pulp, or a portion of devitalizing fiber is used. 
This is then sealed in. 

The cavity should be prepared for the reception of arsenic, decay 
being removed as far as practicable, and the cavity dried. Any 
redundant gum must be pressed away or saturated with trichloracetic 
acid and ablated or removed with the electric cautery. 

In some bad cases with much gum overlying the writer has furnished 
pliers and directed the use of cotton pellets to be dipped into an 
aqueous antiseptic (Listerine, Borine, etc.), warmed in a flame and 
placed in the cavity by the patient. This coincidently sedates the 
pulp. 

There are three good methods of sealing the arsenic. (1) In cases 
not approaching the gum, or where dryness can be maintained, the 
application may be accurately made and quick-setting cement flowed 
over it. This cement is capable of being fairly dropped into a cavity or 
led around the periphery by a probe, and should be very adhesive, also 

1 Dental Cosmos, April, 1917, p. 433. 



442 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 



Fig. 391 



he readily removable. (2) The arsenic may be applied preferably " fiber" 
and a metal or gutta-percha cap (the latter purchasable) placed, liberally 
covering it to prevent pressure, temporary stopping or cement is then 
packed. (3) A still safer method consists in applying a pellet of 
amadou over a part of the pulpal wall. The cement is then introduced 
about the periphery of the cavity, the amadou being left largely 
uncovered. When hard, any cement over the amadou is removed 
and the latter lifted out, thus leaving a box-like receptacle for 
the arsenic and a pellet of cotton partly wet with eugenol in which 
menthol is dissolved. When placed, the orifice is dried and more 
cement added. This method of first making the covering is of special 
advantage when the cavity cervix is near the gum, and prevents the 
forcing of arsenic toward the gum in the act of making the covering. 

Amalgam or facing amalgam 1 or tempo- 
rary stopping may be used in place of the 
cement (Fig. 391). Temporary stopping 
is not very safe against masticatory force. 
In a very difficult case of a distocervical 
cavity with partial pulp death in a lingual 
root the occlusal opening shown in Fig. 
329 was made and an artificial canal con- 
structed as there shown; arsenical fiber 
was then applied to the pulp. 

In another case, in which only a buccal 
wall was standing, the pulp within the open 
canal, a sedative was applied and covered 
with sandarac varnish on cotton to press 
out the gum; after excavation the pulp was 
covered with a pellet of devitalizing fiber 
and this with a pellet of spunk ; over this 
a permanent amalgam and cement combination filling was built. 
This was later perforated to the spunk before thorough hardening. 
This opening was then filled with soft, quick-setting cement. This 
was for subsequent treatment without annoyance. Such a method 
has a wide variety of applications. 

The rubber dam is generally insisted upon, but cannot be. used in 
the worst cases, hence an expert may dispense with it. There is a 
tendency among students to rely upon the rubber dam alone to 
prevent accidents. This is a fallacy, as the same results may occur 
with it as well as without it. The chief danger lies in the use of 
temporary stopping after placing paste. Capillarity and pressure 




Diagram showing method of 
first making the covering for 
an arsenical or sedative appli- 
cation. (See text.) EP, ex- 
posed pulp; AA, arsenical ap- 
plication; C, sedative covering 
to same; A, amalgam placed 
before these applications; A', 
amalgam to seal them in; E, 
enamel. 



Facing amalgam is silver 40, tin 55, zinc 5 parts, and mercury. 



DEVITALIZATION OF THE PULP 443 

often carry the paste to the cervical margin. Making the covering 
first or using fiber constitute the best precautions. 

In case of a very dangerous cavity, as a distocervical one, a special 
drill pit known as a "pocket" is to be made at some other point 
extending in the direction of the pulp horn and as near to it as can 
be made without too much infliction of pain. In this the arsenic is 
to be sealed while antiseptic sedatives are to be placed on cotton in 
the cavity of decay, the first application devitalizes the fibrils and 
permits deeper ones. This method is also valuable when the pulp is 
very irritable, and permits devitalization through a more or less 
healthy portion of pulp. 

The presence of pulp nodules may necessitate an application after 
lifting away the nodule (Fig. 346). 

The arsenical method may be used after a preliminary general 
anesthesia and bulb removal, or may even be used against an obdurate 
pulp canal filament. 

Symptoms. — The large majority of pulps die under arsenic with 
but little pain. Sometimes throbbing pain results, passing into a 
heavy fulness as congestion supervenes. If too great, the pulp should 
be uncovered and bled slightly, then a sedative should be applied, 
iodin used as a counterirritant upon the gum, and pulp death awaited. 
Ordinarily the pain passes away as the pulp becomes more fully 
congested. Apical irritation may result and may be ignored if slight, 
or if severe be treated in the same way as the pulp irritation (Fig. 
354). A guard to prevent overocclusion is sometimes useful but 
seldom required (Fig. 504). 

Accidents from Arsenical Applications. — If a portion of an arsenical 
application escape from beneath its covering, it may destroy much 
or a little gum tissue, according to the amount which escapes. The 
teeth should be seen early in doubtful cases and the condition of 
the gum observed. 

The arsenic may attack the gum festoon, inducing in it stasis 
followed by necrosis. The gum assumes a purplish turgidity, which 
later changes to a dirty yellow slough. 

The bone is usually devitalized for a distance. 

If the necrosis be self-limited, as is usually the case, a small 
sequestrum comes away after a few r weeks. To prevent necrosis of 
the gum, it has been suggested that phenol be applied as arsenic does 
not pass through dead tissue but the slough produced by phenol if 
effectively applied causes doubt as to whether it might be due to arse- 
nic. Care in application is better, any slough to be treated at once. 

In some cases the arsenic may follow the festoon of the gum of 
one or more teeth, causing disagreeable sloughs and ulcerations. 



444 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

It may follow the pericemental tract, kill the pericementum, and the 
tooth drops out. In one case of a boy, aged twelve years, an appli- 
cation was made in a first lower molar. A blow from a base-ball 
was subsequently received and a slight leakage occurred merely a 
trifling slough of the gum being apparent mesially. Later the 
living gum margin appeared flabby and could be lifted away. Finally 
and gradually, during nine months, the buccal pocket deepened 
without loss of the gum, the tooth gradually loosened, the bone 
septum between the roots was found necrosed, the tooth was removed, 
and the socket healed without further necrosis. The alveolar process 
about one or several teeth may be devitalized and a sequestrum 
occur which includes the teeth. Certain toothache nostrums are 
sold which contain arsenic. Dr. G. C. Chance 1 recorded a case of 
arsenical necrosis occurring from this source. Dr. J. E. Powers 2 
recorded a case in which extensive necrosis occurred from the use 
of colored woolen yarn (as a cleanser of interdental spaces) which 
contained arsenic used in the dye. 

Fig. 392 




Boenning's case of coagulation necrosis due to arsenic; shows exposed and blackened 

alveolar process. 

From the infirmary of the Philadelphia Dental College was re- 
ferred to the oral clinic a case of extensive coagulation necrosis, 
resulting from the rubbing of "toothache drops" upon the gum. 
Analysis showed the preparation used contained arsenic. Collapse 
from blood poisoning being the immediate danger, the child was 
operated upon by Prof. Boenning for drainage of the parts. During 
the recovery, the teeth from the right lower cuspid to the left lower 

1 Proceedings of the Academy of Stomatology, Philadelphia, 1898. 

2 International Dental Journal, November, 1902. 



DEVITALIZATION OF THE PULP 445 

second temporary molar, and the gums over the process, were lost, 
leaving a blackened alveolar process, to be later removed surgically 
(Fig. 392). 

Arsenic is liable to pass through the apical foramina of unformed 
or much resorbed roots. It may possibly pass through mature roots 
when an application is placed high up in the canal, rarely when applied 
under normal conditions (as recorded by some), or, as occurred in 
one case, by the application being pushed through the apex. It 
may be forced through in the act of broaching, or through the sub- 
sequent use of the cataphoric current or pressure anesthesia without 
the preliminary precaution of removing the arsenic. 

In some cases arsenic has been applied to perforations made 
through the sides of roots under the impression that the vital tissue 
found was pulp tissue. In such case its necrotic effects will be noted 
upon the gum overlying the root apex or over the perforation, the 
tooth being loosened and extruded and may possibly be lost. 

E. C. Kirk 1 has recorded several cases of loss of teeth from arsenical 
necrosis of the pericemental tissue following the use of mummifying 
paste to pulp stumps previously impregnated with arsenic. His 
theory is that the arsenic was liberated by the affinity of the ingre- 
dients of the mummifying paste for the proteid constituents of the 
pulp tissue. The editor has often used such pastes after arsenic and 
without untoward results, and feels that some other element must 
have entered in Kirk's cases. 

Such dangers as these demand that extreme precautions be taken 
against the careless use of quantities of the agent. The rules laid 
down should be adhered to. 

The only cure of the condition consists in the thorough removal of 
every particle of the arsenic. Any projecting masses of edematous 
sloughing or gum should be cut away, as they are dead and will slough 
at any rate, and a freer access to deep parts is had — the blood-flow 
may itself wash away the arsenic. The forcible washing should be 
prolonged and repeated, or 10 per cent, silver nitrate should be used 
to form arsenite. Tincture of iodin may be applied, with a view to 
possible neutralization of the arsenic, and as a disinfectant. Next, 
euroform paste is applied on cotton and renewed as necessary. The 
mouth is to be kept as aseptic as possible with washes. 

1$ — Orthoform 40 parts 

Europhen 60 parts 

• Liquid petrolatum q. s. — M. (Buckley.) 

The editor, in a case of known application of arsenic to an obscure 

1 Dental Cosmos, October, 1903. 



446 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

perforation, succeeded in causing regeneration of tissue by removing 
surgically the dead tissue and inviting repair. 

It may, therefore, be that after minute portions of arsenic, forced 
through foramina, exert their full effect, the resulting dead tissue 
may be removed by resorption or even exfoliation; indeed, this result 
has been noted in which no other explanation seemed possible. 

If the teeth are loosened and lost as the result of arsenical necrosis, 
either beginning at the gum margin or at the apical space, the alveolus 
will exhibit a bare periphery and even some odor of putrefaction may 
be present. The alveolus should be sterilized and the walls burred 
away to a tissue capable of healthy granulation. 

Special Methods of Preparing Pulps for Removal. — A fully exposed 
pulp in a single-rooted tooth or single root of a multirooted tooth, 
may be suddenly "knocked out" by means of a delicately pointed 
orange-wood stick or Portuguese toothpick. The point is dipped 
in phenol and suddenly and boldly driven into the pulp, either by 
hand or mallet force. The method is not so agreeably delicate as 
pressure anesthesia, but is effective and if completely and accurately 
done, not painful. It must not be used in partial exposure, as, not 
reaching the apex, it may cause pain. Its use is only indicated in 
emergency or occasionally in crown work after excision of the crown 
by excising forceps from which some shock anesthesia may result. 

A vital remnant of pulp may be removed after instilling a strong 
cocain solution, or carbolic acid, or a paste of carbolic acid and 
acetate of morphin, into its substance by means of a "puncture 
probe." This instrument may be made by filing down a Donaldson 
bristle to a fine point, which is further whetted on an oil stone. The 
sides of the probe are polished by folding a cuttle-fish disk upon 
itself, holding it between the thumb and forefinger of the left hand, 
and drawing the probe through it. The pulp canal is flooded with 
the carbolic acid, and gentle thrusts are made into the pulp until the 
probe is stopped at the apex. If it pass through, that must be judged 
by the sense of touch. Custer recommends 75 to 90 per cent, sul- 
phuric acid as superior to carbolic acid. At times a small end of 
pulp filament may be seared with a hot Evans' root drier, which is 
quickly thrust into it. This does not necessarily give much pain. 

A slow but effective method of disposing of these filaments, when 
hyperirritable or when patients are timid, consists in packing a 
cotton twist saturated with carbolic acid containing cocain hydro- 
chloride in solution into contact with the pulp, and then gently 
compressing the pulp. The cotton is to be left in position for a day 
or two to induce thrombosis, when, as a rule, the pulp may be removed. 
A dressing of tincture of iodin has been suggested for the purpose. 



THE EXTIRPATION OF THE PULP 



447 



Erythrophlein Hydrochlorid. — Norman Black (Scot- 
land) introduces 1 throphleol (erythrophlein hyd., 50 
per cent, solution in eugenol), applied on the tiniest 
possible pellet of cotton to the center of the pulpal 
wall of a deep cavity (away from the pulp in old 
exposures or smeared on the pulpal wall of shallow 
cavities, to be tightly sealed in with temporary stop- 
ping or cement for forty-eight hours. He finds the 
pulp as a white, bloodless, insensitive thread with 
tendency to shrinkage ; slight pericemental irritation 
may occur. The application is relatively painless, 
sure and speedy and valuable in cases of intolerant 
patients. Being a powerful drug internally its dosage 
of jq to yV grain should be borne in mind. 

Devitalization of Pulps in Temporary Teeth. — All 
of the anesthetic measures are as applicable to 
temporary teeth as to the permanent ones if the 
little patient will tolerate their application. 

If the child present an exposed pulp in a tooth 
the roots of which are not resorbed, arsenic much 
diluted, may be applied for twenty-four hours and 
then be removed, the pulp being then allowed to die. 
When roots are resorbed B run's cobalt method or 
Black's throphleol method may be warrantable ap- 
plications. Dunbar 2 has advised one or two. appli- 
cations of aqua ammonise on cotton. Pulp capping 
may occasionally be done. 

Darby has used cantharides, Y V grain in carbolic 
acid, with success. It must be carefully sealed, as 
strangury is a possibility. 3 Figs. 35, 43 and 50 are 
guides as to the condition of the end of the root. In 
case of pulp exposure when the root is much resorbed 
only local anesthesia is permissible with such root 
filling as is possible (see pages 475 and 479) ; when 
nearly ready to be shed the tooth is better extracted, 
though capping may be tried if necessary. 

THE EXTIRPATION OF THE PULP. 

The extirpation of the pulp sometimes must be 
immediate for relief of pulpitis. This may be done 
without resort to radiography and after the first 

1 Dental Cosines, April, 1919. 

2 Quoted by Goddard, American Text Book of Oper. Dent. 
8 Dr. J. Foster Flagg had such a case, 



Fig. 393 



Evans'aroot drier. 



448 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

dressing a radiograph taken. At this time the canal may be 
flooded with campho-phenique, etc. and a copper or other metal 
point or strand of picture wire may be passed to the apical region 
and sealed in. The radiograph will then be a still better guide to 
further procedure. 

In cases in which later pulp removal or any canal work is intended 
the radiograph should be taken before the next sitting. In cases of 
apical disease, known or suspected, the radiograph being a means of 
diagnosis should have been previously taken. 

In cases associated with pulp putrefaction formocresol or Howe's 
method should have been used for sterilization as far as may be. 
Thus, what is stated for a vital pulp as to the mechanical opening 
of the canal applies to all cases, except as to indicated antisepsis and 
removal of canal fillings in septic cases. These are explained under 
the various headings. 

For the insurance of asepsis provision should be made for the 
facile adjustment of the rubber dam, in case the cavity extends 
beneath the gum. This may be accomplished by thoroughly excavat- 
ing the cavity and preparing the cervix for a filling. If in posterior 
teeth and amalgam to be eventually used this may be built in per- 
manently after placing spunk or temporary stopping over or into the 
pulp chamber; later this stopping is removed, a germicidal dressing 
placed and canal work done later. An alternative consists of building 
cement temporarily into this wall, another the adjustment of a thin 
ready-made band of German silver with cement or temporary stop- 
ping to enclose the cavity cervix and the tooth. In case of roots 
such a ferrule is adjusted and allowed to protrude above the gum. 
It may remain or be removed at each sitting if in anterior teeth a 
temporary crown be necessary. The use of light clamps such as the 
Palmer set placing the clamp in position and throwing the dam over 
the clamp, adjusting a ligature and the use of the saliva ejector as an 
adjunct complete the rubber dam preparation. (Fig. 485.) 

The field of operation should be sterilized with tincture of iodin 
or phenol followed by 70 per cent, alcohol. Rubber dam not contain- 
ing any starchlike treatment to react with iodin is to be preferred. 
These precautions are supplemented by the use of properly sterilized 
instruments, hands, cotton, paper points, etc., and possibly by 
phenol in the pulp cavity. If napkins must be used, as strict asepsis 
as possible must be employed. This applies also to the pulp anesthe- 
sias (see Chapter on Asepsis). 

Free access to all parts of the pulp cavity and canals must be 
obtained. This is usually best accomplished by an opening made in 
direct line with the axis of the pulp canal. In general terms this 



THE EXTIRPATION OF THE PULP 



449 



involves for sound teeth an opening upon the lingual surface of 
incisors and cuspids and upon the occlusal surface of bicuspids and 
molars. 

This access may consist of a new opening or an extension of a 
cavity, or at times the cavity and canal may simply be made con- 
tinuous. 

When a cavity of decay exists the pulpal wall should be perforated 
and a large bud bur should be used to cut away the dentin over- 
hanging the pulp cavity. It is usually necessary to extend the cavity 
in the central occlusal direction, so as to permit direct access to 
each canal (Figs. 394 to 401). 



Fig. 394 



% 




Fig. 396 



Fig. 397 



$ 





Fig. 398 



Fig. 399 



Fig. 400 



Fig. 401 







When a tooth crown would be irremediably weakened by such a 
course, a slight indirectness is permissible when flexible cleansers 
can be used instead of drills. This leaving of tooth structure should 
be done with judgment. The canals must be cleansed. In cavity 
approaches the outer wall of the pulp cavity should be cut away to 
permit an obtuse-angled approach rather than a right-angled one 
(Figs. 399 and 401). All pulp cavity corners should be burred to 
a shape that obviates retention of pulp debris, the subsequent decom- 
position of which would lead to discoloration and infection. The 
opening shown in Fig. 397, B is faulty for this reason, and is better if 
39 



450 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

extended more toward the incisal edge, making an oblong opening 
with rounded ends. 

In sound teeth the entrance to the canal is made with a small 
spear drill, after the enamel has had a "spot" made in its surface 
with a sharp dentate bur. This centers the spear drill and prevents 
its slipping about. After it has entered the pulp cavity dentate burs 



Fig. 402 



Fig. 403 




i\ 



12 3 4 5 6 


12 3 4 5 6 


XXF XF F M C XC 


XXF XF F M C XC 


Style D 


Style D 


Kerr root canal probes. 


Kerr root canal files. 



are used to enlarge the opening to the desired size and shape. A 
sawing motion creates more rapid clearance and cutting of tooth 
tissue. 

t)ne should not always suppose that the spear drill will drop into 
an appreciable pulp cavity. The careless driving of a drill into a 
tooth may cause a perforation. Secondary dentin or a large nodule, 
and, in previously treated teeth, zinc phosphate may occupy the 



THE EXTIRPATION OF THE PULP 



451 



pulp chamber. Therefore, when doubt arises, open well that portion 
of tooth or filling which has been drilled through, and note the 
conditions, then go ahead carefully. In opening a located pulp 
chamber with burs a bud bur is very useful, but all burs once placed 
through the drill hole and into the pulp chamber must be used 



Fig. 404 



Fig. 405 



Fig. 406 



i 



Donaldson's pulp-canal cleansers. 



Fig. 407 



Fig. 408 



laterally or the heel of the bur used with 
an outward sweep toward the occlusal aspect 
for the sake of safety. 

Large Canals. — The canal (or canals) is 
now to be explored with a fine, sterile, smooth 
broach (Fig. 402), and if of operable size a 
Donaldson cleanser (Fig. 404) is passed to 
the canal apex, twisted so as to engage its 
teeth with the pulp substance, and the pulp 
extirpated. An apexographer or fine barbed 
cleanser somewhat of the Donaldson type 
with a few teeth on the apical end only <j is 
useful in removing a last bit of pulp or defin- 
ing the apical foramen. 

If there be any difficulty in finding the canals 
after preparation of the bulb of the pulp cavity 
by reason of the broach catching on the 

edge of the orifice, the mouth of the canal should be made continuous 
with the wall of the pulp chamber by means of a small bud bur, 
occasionally with a Gates-Glidden drill. The wall then leads the 
broach into the root lumen. Care must be taken not to penetrate 
the side of the root and create a catch for instruments. The Rhein 



Donaldson's spring-tem- 
pered nerve bristles. 



452 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

picks (Fig. 409) being strong probes with sharp points are useful 
in jamming an opening through constrictions at the canal orifice. 

Fig. 409 




Rhein picks. (Courtesy J. W. Ivory.) 

Subsequent enlargements are to be made with Kerr root files 
(Fig. 403) , inserted to full depth and used as a file with outward sweep 
and lateral pressure or with Donaldson cleansers in the same way. 
Fine tapering sizes are first used then the larger ones. 

Fig. 410 



r 






k_j 



Kerr or Downie broaches. Various finer sizes of these broaches and reamers may 
be had. They should have accurate taper. 



Fine Canals. — These usually are fine round or flattened and present 
a difficulty of exploration. To determine direction and penetrability 



THE EXTIRPATION OF THE PULP 453 

the finest Kerr smooth broach, a Young's broach or a Kerr root file filed 
to a fine point is pressed gently toward the apex or moved to and fro. 
If the radiograph shows a root curved the end is bent with sterile 
pliers to conform. Sulphuric acid 30 per cent., sodium potassium 
alloy picked by the broach from its tube, or sodium dioxid taken up 
by the wet broach usually aids in penetration. Much patience may 
be necessary in reaching the apex. A bit of rubber dam as a marker 
may be put on the shank, slipped to a guide point, preferably the 
cutting edge or occlusal surface. 

This depth of penetration may be gauged by the tooth length, as 
shown in the radiograph. In this penetration the side walls of the 
canal support the broach against buckling. Larger sizes of smooth 
broaches should follow; next the finest Kerr root canal files; next 
the larger root canal files or Donaldson cleanser when the canal 
admits them. 

In canal roots only flexible sizes of files and occasionally of Kerr 
twisted broaches can be used without danger of false pockets being 
formed in the sides of the canals. 

When canals are determined and reasonably straight, flexible 
canal engine broaches may be used and where dowels are intended 
root reamers may be used preferably after filling of the apex. When 
it is thought the apex is reached or passed, a sterile diagnostic wire 
is passed and a radiograph made to determine the fact. (Fig 412.) 

When an impasse is reached a diagnostic wire should be placed to 
the point usually after placing a mild antiseptic and sealed in. A 
fresh radiograph is taken and at the next sitting (or the same if neces- 
sary) the work is conducted in accordance with the findings in further 
endeavor to reach the apex either by the same method repeated after 
due lateral enlargement of the orifice of entrance if required for better 
direction or if necessary by drilling through the apex in case a granu- 
loma or abscess must be reached. The object is to remove all organic 
material from the apical portion of the canal and permit the final 
filling in as perfect a manner as possible. A third radiograph may 
even be necessary to determine the accomplishment or the nature 
of the opening made. (Fig. 421.) 

The failure to reach the apical tissue by following the true canals 
or the making of a perforation through the side of a curved root and 
the breaking of the broaches are the dangers to be encountered. 

This operation requires great care and considerable skill and 
involves much time in some teeth. Therefore before undertaking the 
task the patient should be acquainted with the circumstances and the 
work undertaken with full recognition of the possibility of encounter- 
ing these drawbacks and a willingness to accept the outcome. If 



454 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 



compensation is a question, this should be arranged. Should the 
attempt to reach the apical tissues fail after due skill has been em- 
ployed we have an apical end probably containing delta-like openings 
rather than a single main apical foramen, or the fineness or curve 
of the canal has rendered opening impossible. (Fig. 411.) 



Fig. 411 



Fig. 412 





Delta-like canals. (Callahan.) 



Diagnostic wire passing into apical tissue. 



Certain roots may be curved, yet have large canals permitting the 
broach to slide around the curve, while some pretty straight roots have 
very fine operable or inoperable ones. Sometimes the foramen may 
be fair, yet to one side. Thus in a splendid straight root held in the 
hand, I could approach the apex readily and pump the canal contents 



Fig. 413 



Fig. 414 



Fig. 415 



Fig. 416 




through the foramen, but could in no way pass through it even by 
bending the broach. Placing wires and radiographing may help, but 
unfortunately the radiograph is not always a true guide. 

Assuming that one has done all work with conscience, the question 
arises as to the disposition of inoperable root ends. With a possible 



THE EXTIRPATION OF THE PULP 455 

granuloma, apicoectomy (q. v.) or extraction is the indication unless a 
perforation can be made and the case cleared up. This latter only 
when no marked systemic condition is present, time for trial being 
permissible. In fresh extirpations, it seems that one may try pumping 
Callahan's resin (see page 469) into the delta-like foramina or the use 
of a paste and cone after Howe's treatment with ammoniacal silver 
nitrate. (See page 477.) This is on trial. 

In canals of posterior teeth short instruments are mounted in a 
chuck handle and the shank sharply bent at a right or obtuse angle 
or soft soldered into a small ball of metal and used straight or used in 
the longer handle or the Kerr thumb knob may be grasped in a Jack 
porte. If used short the fingers used should be dipped in 1 per cent, 
iodin trichlorid. If the cleanser bind in the canal, it should be grasped 
with the thumb and forefinger and given a straight pull to relieve it. 

If acid be used it should be neutralized 
with sodium bicarbonate or sodium dioxid. Fig. 417 

The improved Gates-Glidden drill (Fig. 
417) has some use in the enlargement of 
canals the lumen of which has been de- 
termined by the above methods. They 
should not be used for the preliminary 
opening of fine canals except at the orifice, 
as they tend to form false channels in the improved Gates-Glidden 

. . p . ii-i i i nerve-canal drill for engine 

side or the canals which constantly catch wor k. 

even fine bristles and may render a canal 

into a form even less advantageous than that it already possesses. 

The canal filament of pulps in molars and upper first bicuspids may 

be^lifted^away with barbed broaches or cleansers if the canals are 

large, but it is ordinarily a waste of time to attempt it in the finer 

canals, as the other work must be done in the apical regions. 

The use of 5 per cent, formalin, tannin, or alum, to be specially 
applied about two days after the application of arsenic, has been 
suggested for the toughening of pulps. Their use necessitates a visit 
for their special application. They toughen the pulp, and, while 
the advantage in pulp removal is offset by the special visit needed, 
may, in fine canals, mummify inaccessible portions of pulp tissue. 

The scraping of the canals removes the possible remnants of 
pulp tissue, odontoblasts, etc., adhering to the dentin walls, and 
also a part of the wall with the large ends of the fibrils. All these 
are decomposable media, may become septic, and are wisely removed. 

The final removal of all pulp debris, coagulated blood, etc., is best 
done with a fine Donaldson cleanser, moved to and fro in the canal 
with one hand, while with the other a stream of warm sterile water is 



456 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

gently introduced by means of a Moffat syringe. A large cottonoid 
roll or a napkin may be held by the patient or assistant to absorb 
the excess of moisture when the rubber dam is in position. When 
cotton twists are to be used they should be would with fingers 
dipped in H 2 2 plus mercuric chlorid (1 to 500) as suggested by 
Ottolengui. He states that such a treatment is safe. One per cent, 
iodin trichlorid may also serve. 



DESCRIPTION OF FIGS. 418, 419 AND 420. 1 

Fig. 418. — Fig. 3 gives in contrast a sectional view of deciduous and permanent upper 
teeth divided through their lateral diameters. 

Fig. 4, a sectional view of the corresponding lower teeth divided through their 
anteroposterior diameters: a, b, c represent respectively the deciduous and permanent 
front incisors in contrast; d, e, f, the lateral incisors; g, h, i, the canines; k, deciduous 
molars, upper and lower; I, m, the successors to the deciduous molars, the bicuspids; 
n, o, represent permanent molars; c,f, i, m, o, have dotted lines indicating the thickness 
of enamel removed by wear, atrophy of the cementum, and reduction in the size of the 
pulp due to progressive calcification, these changes being incident to old age. 

Fig. 419 erpresents in Fig. 1, letters a to h and a to h, the longitudinal or vertical 
sections of the sixteen upper teeth, showing the labiopalatal diameter of the pulp 
chamber and canal in crown and roots, the section of the molars being through the 
anterior buccal and palatal roots, while the bicuspids d e and de illustrate the result 
of such a compression of the root as to divide the pulp chamber into two canals — a 
condition which so frequently exists in these flattened roots. The double-lettered 
series, d d to h h and dd to hh, represent in the molars a section through the posterior 
buccal and the palatal roots, from which is quite readily recognized the slightly greater 
lateral diameter of the pulp chamber in the crown and the larger canal in the posterior 
buccal root over that in the anterior buccal root, while the bicuspids lettered e e d d 
and dd e e illustrate modified pulp chamber and canal, with bifurcation of the root- 
in one, these being cut through a different axis or plane from the single-lettered series. 

Fig. 2, letters a to h and a to h, represent the sixteen lower teeth with the section 
through their long diameters, as in the upper series. These incisors illustrate the 
compressed or flattened condition of their roots in contrast with the cylindrical char- 
acter of the roots of the upper incisors, while the bicuspids d e and d_e illustrate the 
singleness of their pulp chamber and the cylindrical condition of their roots as in 
contrast with the flattened or compressed condition of the roots of the upper bicuspids. 
The molars /, g, h, and /, g, h represent sections through the anterior root, illustrating 
its compressed condition and divided pulp chamber in the first and second molar, 
and a somewhat flattened one in the anterior root of the third molar; ff,gg, hh and 
/ /. g,hh represent the single and cylindrical pulp chamber in the posterior root of 
the lower molars, while b b, c c and a a, bb represent the incisors and canines of the 
same series, with modified pulp chambers arising from modified development. 

Fig. 420. — Fig. 1, from a to h and a to h, represent the upper teeth, with transverse 
or horizontal section through the base of the pulp chamber in the crown, viewing 
the entrance to the canals of the several roots, while the same letters in Fig. 2 represent 
the lower series in the same manner. 

Fig. 3 represents the upper teeth, with the transverse or horizontal section made 
below the largest diameter of the pulp chamber and through the canals after they 
have diverged from the central chamber, but before the roots into which they run have 
in the molars bifurcated. 

Fig. 4 in like manner represents the lower series, well illustrating the flattened or 
compressed condition of the canal anterior roots of the molars and the division of the 
chamber, as is frequently found in the roots of the lower incisors. 

The letters aa,bb, cc, dd, f f, d d, and e_e (Fig. 3) represent the relative shapes, 
whether circular, oval, or flattened, of the pulp canal in the roots of the upper central 
and lateral incisors, the canines, the first and second bicuspids, and the first, second, 
and third molars, while the same letters in Fig. 4 represent the relative shapes of the 
pulp canal in similar teeth in the lower series. 

1 These figures are taken from v. Carabelli 's Anatomie des Mundes. 








45" 




458 



A 




a - 



»/ CO 



p 



$ 




s 



§ 



& 




fip 




// 



*/] 



-wm. 














JJJISS'P 



% 



e e 




H 6 









feb 






/ 



4(H) REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

Tempered Swiss broaches or prepared bristles are -best for handling 
cottons though the Kerr broach will serve occasionally. 



Distal - 




Fig. 422 Fig. 423 Fig. 424 



mesial 



Diagram illustrating the improvement in ac- 
cess C, to the deeper portions of enamel by cut- 
ting in accordance with a radiograph. The 
dotted line shows the ordinary opening per- 
mitting the access b b. (Rhein.) 




Upper lateral incisors. (Otto- 
lengui). 



Fig. 425 



Fig. 426 



Fig. 421 





Fig. 428 



Upper canines. 
Fig. 429 





Fig. 430 




/ W 

Upper first bicuspids. 

When the broach must be bent to enter canals, loosen the broach 
first before introducing into the canal, thus leaving the cotton 
loosely mounted on the broach. To prepare a Donaldson bristle cut 
off the hook and flatten the end upon an Arkansas stone, and slightly 



THE EXTIRPATION OF THE PULP 



401 



flatten on two sides, then lay upon a glass slab and burnish thor- 
oughly to remove any bur left. In use the cotton and broach are 
rolled with the left forefinger and thumb only. It is obvious that 
to do this the broach must be perfectly straight. When slightly 
bent the method of rolling the cotton next described may be em- 
ployed. The writer believes the prepared Swiss broach not only 
more facile but economical in use. 



Fig. 431 



Fig. 432 





b a 

Upper second bicuspid. 



b a 

Upper first molar. 



Fig. 433 



Fig. 434 



Fig. 435 






Upper molar. 



b . a 

Upper second molars. 



To prepare broaches, select accurately tapering Swiss or English 
broaches from which the temper has not been drawn. Next, draw 
the temper by placing a few in a test-tube and heating first at the 
shank, gradually drawing the tube over the flame toward the points. 
The blue color seen on the shank should be run out to the tip; let 
cool on any open surface. The soft broaches usually sold are nearly 
useless. The point is left if canal exploration is intended. For 
carrying cotton twists, cut the end off with scissors. To wind the 
cotton lay a wisp on the left forefinger, lay the broach upon it, close 
down the thumb, then quickly revolve the broach with the right 
forefinger and thumb, pushing the cotton through those of the left 
hand to form a symmetrical cone. To use as a swab, rotate in the 
canal to the right. To leave the cotton in the canal, rotate to the 
right as the twist is pressed to the apex. Then turn the broach once 



402 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

or twice to the left to loosen it from the cotton, withdraw a little, 
then press in again. Thus the cotton is crimped upon itself. 

The forms of normal pulp cavities and varieties of abnormal root 
are shown in Figs. 418 to 451. 

In fresh pulp removals a sedative, such as campho-phenique plus 
menthol should be sealed in until healing is assured when the root is 
to be filled. 

In cases originally septic the treatment is continued as indicated 
under pulp putrefaction, apical abscess, etc. (See page 493.) 



Fig. 436 



Fig. 437 



Fig. 438 






Fig. 439 



Fig. 440 



Fig. 441 






Upper molars. (Ottolengui.) 



Fig. 442 



Fig. 443 




Q 




Upper third molars. 



The carrying out of canal treatment involves a knowledge of the 
topographical anatomy of the teeth and their pulp canals. As an 
aid to this Figs. 418, 419, and 420 are introduced, showing the normal 
outlines of the teeth and their pulp chambers. 

In a few cases in which cervical cavities obliterate the canal or 
cause annoying approach to it, it is desirable to remedy the con- 



THE EXTIRPATION OF THE PULP 



463 



dition. In such case the canals are opened as usual and enlarged, 
and the cavity prepared with suitable retentions for filling. The 



Fig. 444 




Fig. 445 




Lower bicuspids. 



Fig. 446 





Lower first molar. 

Fig. 450 





Lower first molar, immature. 
Fig. 451 




Lower second molar. 



Lower third molar. 



last-used reamer is then to be placed in the canal and the filling 
inserted. The filling is then supported by pressure while the reamer 




404 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

is slowly twisted to the right and withdrawn, leaving a canal through 
the filling. This may be done with amalgam or with zinc phosphate 

if a later removal be required. If the 
FlG 452 root be much weakened, a tapering dowel 

may be cemented through the crown 
and canal, thus attaching the root to the 
crown more firmly (Fig. 452, also page 354). 
If intended the dowel is used as the canal 
former instead of the reamer. 

ACCIDENTS IN CANAL OPENING. 

The chief accidents that may occur are 
the perforation of the root wall and the 
breaking of the instruments used. If the 
canaTcontinuity rcS The canity technique laid down be carefully followed 
should have more retention the danger of perforation is practically 
own.a,amagam. e li mma t e d. In fact, the greatest danger 
is the penetration and enlargement of the 
apical foramen, occasionally of lateral perforation near the apex 
(Fig. 468). Accidents are usually the result of thoughtless forward 
pressure of reamers and drills, and care will reduce this to a minimum. 
Sometimes one must take the chances with the Kerr engine or hand 
reamer, especially when the shapes of roots are known and an abscess 
must be reached. When doubt exists as to canal locations, the desic- 
cation of the pulp chamber is of great assistance by bringing them 
into view, and if secondary deposits exist one should always use a 
small bud bur and keep well within the limits of the dentin of a root 
while gently seeking a canal lumen. 

Frequent exploration should follow gentle advances, and, as a 
rule, the canal will be found of fairly normal size just beyond the 
point of constriction. In some cases 50 per cent, sulphuric acid 
should be sealed against the suspected canal and the operation 
deferred to another sitting. 

If a perforation be accidentally made in the lower part of the canal 
it may be treated as shown on page 350 and kept under observation. 
One should use every means to diagnose such an opening if not 
plainly such and arsenic should never be applied to one. Cases of 
extensive necrosis have occurred from carelessness in this direction. 
It may be that the low perforations should not be filled, but if canal 
filling is admissible at all the opening should be sufficiently large and 
cone-shaped throughout to admit a fair sized truncated cone handled 
as for cases of large foramina (p. 472) and the end finally smoothly 



ACCIDENTS IN CANAL OPENING 



465 



Fig. 453 



bevelled. Lead cones may also be used. Radiography will deter- 
mine if properly arranged. High perforations leave little to be done 
except apicoectomy or reimplantation if consented to or desirable. 
The breakage of broaches is largely avoidable through the use of new 
instruments and by adhering to the rule of using the smaller sizes 
of unbarbed broaches until the canals are suffi- 
ciently enlarged to permit the use of larger 
sizes, and, in case of engine reamers, of start- 
ing the power with the reamer loose in the 
canal. The "pull" of an engine reamer must 
be borne in mind to avoid undue apical en- 
largement. The engine broach seems to be 
of better temper than the engine reamer. 

Accidents of this sort usually occur with 
barbed instruments of the Donaldson cleanser 
type, especially when used with force. 
Sulphuric acid tends to disintegrate the 
broach, so that lactic acid is often better 
used with it, or the alloy of sodium and 
potassium with a smooth broach will open 
the canal so that the cleanser will not bind. 
If it does it should be grasped with the 
thumb and finger and given a straight pull. 

While avoidance is far better than the ap- 
plication of the remedy, if the accident occur, 
the broach should be removed if possible. 

If lying loosely in the canal a new root file 
may be passed to one side of it and then a 
barbed cleanser pressed against it. It should 
engage the barbs and jig it out. 

Cotton wrapped on a small Swiss broach 
may be pressed down at one side of the 
broken broach and its fibers made to engage 
its barbs. 

Moving the broach back and forth while 
sulphuric acid, sodium dioxid, or sodium and 
potassium is about it, will sometimes loosen 
it. One may sometimes drill to one side of a 

broken instrument with a Kerr hand broach in order to more readily 
engage it with a barbed instrument. If very loose a magnetized 
probe will attract it and draw it out. 

If the broach be tightly fixed in the canal, sodium chlorid, tinc- 
ture of iodin, sulphuric acid, aqua regia, or 25 per cent, pyrozone 
30 



Split and threaded in- 
strument for engaging 
the shank of a Gates- 
Glidden drill. 



466 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

may be sealed in, in the hope of chemically disintegrating it. Milton 
J. Waas 1 recommends the application of 25 per cent, aqueous solu- 
tion of trichlorid of iodin for three minutes to form soluble ferrous 
iodid and chlorid— drying and picking with Rhein picks — drilling 
alongside if safe, extending the surface of application, repeating as 
necessary. For anterior teeth a coating of paraffin within coronal 
dentin to prevent discoloration. 

The head of a Gates-Glidden drill or Kerr reamer is treated in the 
same manner. Sometimes in straight roots the How applicance 
shown in Fig. 453 is useful. If any broach be irremovable, there seems 
to be no alternative except tentative treatment (as on page 475) or 
apicoectomy, reimplantation or extraction. 

The quality of the Kerr root files together with their taper renders 
their use of great advantage over barbed instruments, though these 
are occasionally useful. 

THE FILLING OF ROOT CANALS. 

The opening of root canals as described to this point, leaves us 
two conditions which have to be considered: 

1. The root canal has been opened to the apical tissue. 

2. Such opening after conscientious work has been found im- 
possible. 

To determine the success of the operation a wire is to be placed 
in the canal and a radiograph secured. The cone to be used, whether 
of gutta-percha or metal, may be inserted to full penetration with 
an aqueous antiseptic and sealed with its lower end accessible for 
removal. The radiograph will show the modifications necessary. 
This together with the character of the canal as determined while 
scraping are the only data for guidance in root filling. 

The object is to tightly seal the canal exactly to the apical tissue, 
though it has been determined that chloro-percha and even an 
accidentally extended gutta-percha cone is not irritant after the first 
mechanical disturbance and chemical irritation from the chloroform. 

The reason for complete filling is the prevention of the presence in 
any part of the canal of organic matter, pulp remnant, apical fluid 
or fluid from the crown, which may offer nutrient medium for bacteria 
or any spaces that may admit them. 

It is here assumed that by disinfectant treatment any present 
septic conditions shall have previously been removed. (See Pulp 
Gangrene, etc.) 

1 Fully described in Dental Cosmos, October, 1918, and Dental Items of Interest, 
March, 1918. Obtainable from Merck & Co., New York. 



THE FILLING OF ROOT CANALS 467 

If possible, it is additionally desirable to so saturate the dentinal 
tubules opening into the root as to prevent ingress of bacteria to 
them or egress of any accidentally harbored in that situation. 

Normal Well-opened Canals. — The materials considered best for 
the complete filling of these are chloro-percha and gutta-percha cones 
combined or a solution of violin resin and gutta-percha cones. 

Chloro-percha. — A syrupy solution of gutta-percha base plate 
(G. P. plus zinc oxid) in chloroform which is a disinfectant in itself. 
The writer prefers an addition of iodoform or aristol to maintain 
asepsis after the dissipation of the chloroform, but many prefer to 
rely upon strict asepsis only which should be adhered to in any case. 
A small addition of bismuth trioxid to increase radiopacity has been 
suggested by Davis 1 to overcome its occasional radiolucency . Kells 2 
denies this but I have certainly followed a gutta-percha root filling 
further than shown in the radiograph. 

A further variant consists in the use of ductile temporary stopping, 
which has been melted in a spoon and with which about a fourth of 
its bulk of aristol is incorporated. These are rolled, under sterile 
precautions, on a glass slab with a broad spatula to cone shape and 
kept in bottles containing a paraform tablet, etc. They are more 
readily compacted in canals than gutta-percha cones. The writer 
prefers the qualities of the S. S. White temporary stopping for this 
purpose. 

Gutta-percha Cones. — These are diagonally cut portions of gutta- 
percha base plate rolled while warm upon a slab with a flat instrument 
like an ivory paper cutter or broad steel spatula. It is well to have 
them quite long and to flatten the larger end with pliers to facilitate 
handling with pliers if desired. They are to be kept in 70 per cent, 
alcohol or 10 per cent, formaldehyd solution or subjected to dichlora- 
mine-T vapor, etc. (See Asepsis.) 

In an experimental study of the tightness of gutta-percha root 
fillings, made under exceptionally favorable conditions, and even using 
rosin in chloroform, Price 3 found them not to make such a sealing 
of canals as to prevent the possible entrance of bacteria. If they 
are to be used some lute must be found which shall better prevent 
infection. 

While this seems a laboratory result it is clinically a fact that roots 
filled with gutta-percha can be handled for crown work and bear 
temporary crowns set with base plate gutta-percha over quite a 
period. Many roots partially filled give no sign of abscess or granu- 



1 Dental Cosmos, May, 1918. 2 Ibid., July, 1918. 

3 Journal National Dental Association, December, 1918. 



468 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

loma. Also many granulomas, etc., clear up on proper sterilization 
and its use, so that we must await further evidence. 

Metal Cones.— A variant in cones for special purposes is a silver, 
zinc or copper cone or sometimes the last Kerr root file used in 
enlarging the canal. 



Fig. 454 



Fig. 455 





Kerr root files, used as diagnostic wires 
and later as root canal cones. 



Lateral root slightly capped at end. 
Cuspid root not completely filled, due 
to root curve and offset in canal. 
Amalgam used to repair a peculiar 
split, causing gingivitis, due to over- 
hang. 



Fig. 456 



Fig. 457 




Abscessed right central, left central 
normal for years with cone penetrating 
apical tissue. 




Right central filled with single cone 
and chloro-percha, with aristol. Very 
large inlay, with dowel, due to fracture. 
Fresh pulp removal. 



The writer used the Kerr files employed in scraping the roots in 
the case shown in Fig. 454. These files remained in the position 
shown for several weeks, while I was ill, without irritation. The 
abscesses even improved. Taking the radio as a guide I cut off the 
surplus and after pumping chloro-percha reintroduced them in their 
respective roots. This was done as a desperate experimental resort, 
the lingual root having pyorrhea to the apex. Incidentally this was 
the easiest opened molar I have ever treated. 



THE FILLING OF ROOT CANALS 469 

Colophony. — Callahan recommends violin resin, grains 12, in chloro- 
form 3 drams, as a thin varnish for filling the desiccated tubuli. 
The canal is filled with the solution and the gutta-percha cone 
pumped back and forth forty to sixty times to dissolve the cone and 
force the resultant mixture through the apical foramen and even 
multiple foramina. The cone, or a fresh one, is then packed in with 
pluggers touched to a cake of paraffin. 

The cone is liable to curl up under this pumping action so that a 
fresh cone might be used after the first few pumpings. 

When chloro-percha is to be used the desiccated tubuli may be 
saturated with iodoform in alcohol, aristol in chloroform or mercuric 
chlorid 1 to 500 in hydrogen dioxid or Callahan's resin solution may 
be pumped in before applying the chloro-percha. 

Crane 1 recommends that when it is desired not to pass the foramen, 
a small cone be used with a stirring motion rather than a pumping 
one to get a solution, then a larger but easy passing cone is used, 
dipped in the resin solution and passed almost to the end. Time is 
allowed for the chloroform to evaporate and the cone to soften. 
It is then packed with a blunt canal plugger until sensation is first 
felt. 

A fine plugger is warmed, used to press the cone laterally, and this 
space then filled with a cone. If incompletely done it is softened by 
chloroform and repacked without removal. 

When desirable to cap the root end, as many cones as are neces- 
sary to form sufficient semifluid are used with pumping motion. 
A cone is placed, allowed to soften, packed with the blunt plugger to 
sensation and the patient allowed to bite on a lead pencil eraser to 
force back the soft filling solution around the root end. 

In the use of chloro-percha and cones, the former is carried in on a 
Kerr file, etc., and pumped down (or on cotton wound on a Swiss 
broach). The cone previously tried for proper penetration and dried 
is cut off at say, a half inch length and deposited in the canal with 
sterile grooved pliers and pushed slowly toward the apex with the 
largest admissible flat-ended canal plugger, followed by other sizes 
until it is packed solidly in the apical region. 

If sensation is produced the canal may be filled with other sections 
of the cone, each taking up some of the chloroform. If no sensation has 
been produced the remainder of the canal may have a pellet of sterile 
cotton placed in it and sealed in. 

A radiograph is made, and, if necessary, the cone may be further 
driven in by malleting a canal plugger as suggested by Ottolengui. 

1 Dental Cosmos, 1918, p. 1G99. 



470 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

In large canals one is liable to lose a section of cone and I prefer 
first to try a long, large tapering cone, cutting off the apical end if 
sensation is produced. 



Fig. 458 



Fig. 459 





Cone well placed at apex, with space 
alongside at middle third. This permitted 
passage of a small broach for a distance. 



Temporarily crowned central and lat- 
eral, with rarified apical tissue. Cones 
passing through foramina. Cuspid ab- 
scess, with fistula and consolidated root 
end later drilled through. 



Fig. 460 



Fig. 461 




Same as Fig. 459. Later date, apical 
tissues improved. Formocresol treat- 
ment. 




Root canal filling, twenty-one years 
old, done after incomplete devitalization 
by arsenic, with slightly painful pulp 
removal. Healthy apical tissue. 



Chloro-percha is now pumped in, and the cone gently pressed in to 
sensation. This is pressed aside and a second cone introduced, a 
third, if necessary. The whole is warmed with hot air and gently 
packed. A single cone is liable to leave a space at its side. 

Oxychlorid of zinc is placed in the bulb of the pulp cavity. 



THE FILLING OF ROOT CANALS 



471 



Ottolengui 1 states that chloro-percha, experimentally used, adheres 
to a wet root a"pex. 

Some controversy exists as to the passage of chloro-percha out 
of the foramen. It would seem that the irritation produced subsides, 
the chloro-percha becoming encapsulated and tolerated. 



Fig. 462 



Fig. 463 





Good old root canal filling. No history. 
Fig. 464 



Gutta-percha cone placed at eight 
years of age. Twenty-one years in 
place and comfortable. Peculiar ap- 
pearance not apparently a rarefaction. 
Fresh pulp removal. 



Fig. 465 





Successful root filling, not going 
to end of root. 



Recent root canal filling in slight excess 
Some pericementitis on treatment for pulp 
putrefaction, some following canal filling; 
now comfortable. The bone in radio- 
lucent area shows better than in the re- 
production, which would look like exten- 
sive abscess. In fact, sensation was 
produced by the chloro-percha. 



Figs. 459 and 460 show the passage of cones through the foramen, 
probably to a position rendering them irremovable. A later radio- 
gram shows their toleration. Incidentally these teeth were highly 
infected open roots, repeatedly treated with formocresol and tem- 



Statement before Pennsylvania State Dental Society, 1917. 



472 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

porarily crowned for weeks. These roots are comfortable at present 
with porcelain faced crowns mounted on them. The fistula on the 
cuspid has healed. Fistulas rarely show w T ell in radiographs. 

Euca-percha. — The basis of this substance is a solution of gutta- 
percha base-plate in eucalyptol. To this various antiseptics may 
be added. There are various modes of making this substance. 
B. L. Cochran 1 suggests the following: 

Ifc — Gutta-percha base-plate • . . . §ss 

Dissolve in chloroform q. s. to a thin solution. 

Add saturated solution of thymol in eucalyptol . . . fgss 
Let the chloroform evaporate. 

Euca-percha Compound (Buckley, Lilly) is a simple solution of 
base-plate in eucalyptol made by aid of heat. 

Formo-percha (Blair) has paraform and oil of cassia added. 

This material may be warmed into a creamy paste and be used 
either on cotton or be used in conjunction with gutta-percha 
cones. 

Oxychlorid of Zinc. — The use of oxychlorid of zinc cement pumped 
into the root has long had a value. The zinc chlorid is antiseptic. 
The chief objection lies in its being a cement which is always difficult 
to introduce against the air column, i. e., the filling is apt to be 
imperfect. 

Custer proposes a novel method. ' 'A long zinc cone is used to intro- 
duce oxychlorid of zinc with which precipitated metallic zinc has been 
incorporated to make it a conductor of electricity in future treat- 
ments by electrolysis if needed." While described for the treatment of 
infected roots after electrolytic treatment (see Pulp Gangrene), it 
should have a value if it can be shown to be effective. The oxychlorid 
is pumped in and the zinc cone left in and cut off in the pulp cavity 
in an accessible position. According to Custer's idea if granuloma 
recurs the zinc cone is to be uncovered and galvanic electricity applied. 

Roots with Open Foramina. — These may be incomplete roots with 
very large apical openings, in which case wax with aristol is the best 
filling used, as previously stated. It should be said again, however, 
that if possible the pulp of such a tooth should be capped to permit 
root formation to be completed. 

If the foramen is of moderate extent and either natural or unfor- 
tunately made with drills, gutta-percha cones are valuable. 

A long, tapering cone is prepared. Some point on this must fit 
the foramen. It is tried in and as often as sensation is felt it is 
cut off a trifle and tried again until it chokes the foramen without 
sensation. 



THE FILLING OF ROOT CANALS 



473 



In case of abscess, or even in fresh pulp removals, this may extend 
beyond the apex of the tooth. 

The cone should be marked at a point corresponding to a guide 
point chosen and be laid aside. Next, a fine hook made by bending 
the tip of a fine broach to a right angle, then cutting it close to the 
shank, has a piece of rubber dam slipped over it and is passed through 
the apex and hooked upon the edge (Fig. 466). The dam is slipped 
to the chosen guide point. The probe hook is withdrawn, the dam 
laid at the mark on the cone, and the cone cut off at the lower edge 
of the hook (Fig. 466, b). It should be firmly placed or even sealed in 
position with the end accessible and radiographed. The protruding 
end is cut off. In use, a little solvent, preferably chloro-percha plus 
aristol, is placed in the canal and the cone slowly slipped to place 
until the mark coincides with the guide point. The cone is then cut 
off with a hot instrument, warmed, and gently packed into the canal. 
A section may be used. Fig. 463 is from a case so treated. 



Fig. 466 



Fig. 467 




-b 



Manner of measuring the length of a root 
and fitting a gutta-percha cone. 



Manner of tapering a canal to fit 
cone of the same size. 



When the canal has been reamed with a small engine reamer, and 
the apex enlarged, thus having parallel sides, it is advisable to make 
it cone shaped. The hook may be placed and have a bit of rubber 
dam on it as a guide. Then slip a bit of dam over a larger tapering 
root reamer at a corresponding length. Drive the reamer in until at 
the guide point. The cone is then constructed as above described. 
(Fig. 467). 

In some cases of large foramina or perforation a bit of sterile 
grafting sponge may be introduced into the apical space and the 
filling placed against it. 1 This has not been tested by radiography. 

1 G. Brunton, England: Dental Cosmos, 1900. 



474 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

Wax or Paraffin. — Either of these may have a portion of thymol, 
aristol, or iodoform added to it while melted in a spoon. It is 
then rolled into cones. In use a cone is dropped into the dried pulp 
chamber and a hot Evans root drier point applied. As it melts, the 
metal point is carried down into the root and the fluid material 
pumped to the apex. Capillarity does part of the work. It adjusts 
itself to the tissue and the canal walls. The pulp chamber is then 
cleared of excess wax, etc., and filled without pressure. 

Prinz 1 recommends the use of hard paraffin having a melting 
point of not less than 132° F. in the following combination: 

I*— Thymol 2 parts 

Bismuth trioxid 30 parts 

Hard paraffin 68 parts 



Fig. 468 



Fig. 469 




A, perforation through side of apex; 
D, cone of gutta-percha passing through. 




Lateral perforation due to holding a 
bur at a wrong angle to the axis of the 
root: A, root canal subsequently filled 
with gutta-percha ; B, perforation filled 
with a fitted cone of gutta-percha; C, 
zinc oxy-chlorid. 



The canal is to be thoroughly dried, then merely moistened with 
liquid paraffin, a cone of the compound then to be placed in the 
canal and melted with a root drier (an electric drier or Evans' or 
Reithmuller's modification, 2 Fig. 393). The paraffin combines with 
it and leads it to place with exclusion of air. The bismuth is added 
to make it impervious to the a>rays, hence it throws a radiographic 
shadow. 

The paraffin seems occasionally to disappear from canals. Dr. 
Edwin Shoemaker demonstrated one case in which a root shown well 
filled with paraffin in one radiograph had apparently lost a con- 
siderable portion as shown by a succeeding radiograph. To what 
extent this is true as also claimed by Reithmuller 4 is not known nor 

1 Dental Cosmos, October, 1912, p. 1089. 2 Ibid., March, 1913, p. 342. 

3 Not published in his paper in Dental Cosmos, May, 1917, but shown at Academy 
of Stomatology. 

4 Private Communication. 



The filling of root canals 475 

is it certain whether it is an absorption or a case of original non- 
placement. Reithmuller claims that the radiograph demonstrated 
good filling, but that subsequently it had disappeared. In Shoe- 
maker's case there was no evidence of tissue entering the root canal. 
In my use of wax plus thymol I have later found canals unfilled at 
the apical end. I believe the air cushion makes the difficulty. 

Salol and Thymol. — Both these solid antiseptics melt above body 
temperature and should theoretically be perfect root fillings when 
melted in roots. They are subject to disappearance as above noted, 
with paraffin. The writer tried thymol with cotton to be certain of 
placement, but later the cotton was found limp and easily removable 
with a barbed broach. 

Silver Deposition. — Howe claims that an insoluble silver deposition 
may be deposited in apical deltoid or fine inaccessible foramina. The 
method is described in full on page 477. 

Inoperable Apices. — Various remedies for multiple foramina have 
been suggested. 

1. The method of Callahan, pumping thin violin resin solution, 
the chloroform of which also dissolves the gutta-percha creating a 
mixture. This has just been referred to (page 469). 

2. Malleting the cone upon chloro-percha previously introduced 
to force it sidewise if the foramina happen to be lateral. 

Fig. 411 shows multiple foramina considered by Callahan to be 
present in a large percentage of molars. 

3. Filling solidly with gutta-percha and chloro-percha to the part 
or with oxychlorid of zinc and a cone of gutta-percha (Prinz) and 
subsequent apicoectomy (q. v.). 

4. Extraction, root filling, exsection of the root end and reimplan- 
tation. 

5. The use of iodoform paste, oxpara, mummifying paste or similar 
substance packed alone or in connection with a cone of gutta-percha. 

6. The Howe Treatment and Filling. (See page 477.) 

7. Extraction as incurable (especially in abscess cases.) 

These methods, with perhaps the exception of apicoectomy, may 
be considered sub judice with much disfavor shown them particularly 
as to use of pastes. 

Grieves 2 makes the statement that his radiographic observations 
show that such cases as have had mummifying pastes used have 
very infrequently shown granulomas. He disclaims advocacy of the 
practice. Hundreds of radiographs showing canals only partly filled 
with gutta-percha, etc., show no granulomas. 

1 Journal of National Dental Association. 1917, p. 167. 

2 Ibid., August, 1918. p. 788. 



470 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

It would seem fair that this subject should be threshed out by 
carefully conducted cases before the method should be condemned 
in this class of cases, especially if kept under radiographic observa- 
tion. (See Mummifying Pastes.) 

The Howe method, of infiltrating the multiple foramina and tubuli 
with a sterilizing silver deposit seems worthy of extended experi- 
mentation. 

Fig. 470 




Levy's pulp canal pluggers. 



Canal Pastes. — The pastes which I have used are iodoform paste 
and mummifying pastes. I am not able to certify to the status of 
these materials, but believe their use is occasionally justified in molars. 

Iodoform Paste. — To a resinous solution (made by adding resin to 
formocresol and removing the water which separates), iodoform and 
bismuth subnitrate or trioxid may be added. The thin solution or 
cresol alone, is first pumped in to exclude air. Then thick, freshly- 
made paste is gradually pumped down and the whole compressed 
with cotton to absorb the moisture and either left in that condition 
or a cone of gutta-percha introduced. Oxyeugenol plus aristol, then 
a cone, is commended by Howe after his silver treatment, but 
iodoform may be substituted. 

Mummifying Paste. — There are several formulae for this: 

T$ — Paraform 1 part 

Thymol 1 part 

Glycerin 1 part 

Zinc oxid 1 part or more. 

Or, 

]$ — Paraform 1 part 

Thymol 2 parts 

Alum 1 part 

Zinc oxid 2 parts 

Creosote to a thick or thin paste. 



THE FILLING OF ROOT CANALS 477 

This is used as a temporary germicidal canal dressing on cotton 
or as a root-filling with gutta-percha or temporary stopping cones 
which are pressed into it. 

Fig. 471 




Root-canal filling: A, gutta-percha; B, zinc oxychlorid. 

Soderberg 1 recommended a paste composed as follows: 

1$ — Alum exsic, 
Thymol, 

Glycerol aa 5J 

Zinci oxidi q.s. to make a stiff paste — M. 

It is preferable to add the zinc oxid as needed or to make a small 
quantity of the paste frequently, as it gradually hardens. To the 
paste used a crystal of cocain is added to prevent pain. Bennette, of 
England, has advised the use of paraform incorporated in the paste, 
for its well-known antiseptic and hardening effects. Greenbaum 
suggested the use of a drop of 40 per cent, formaldehyd solution to be 
incorporated with the paste. Both reduce the pulp to the consistence 
of catgut. 

Soderberg reopened cases months after application of the paste to 
pulp stumps, and found them shrunken and with an odor of thymol 
about them. It is not recommended to use this other than as a 
canal filling. 

These would be used as antiseptic pastes in all cases and addi- 
tionally as mummifying agents in inoperable apices containing a 
vital filament of pulp. 

All such cases should be provisionally filled with the understanding 
that extraction is to be resorted to if granuloma arises. 

Howe Method. — Howe's method of infiltrating apical deltoid or 
fine inoperable foramina has aroused much interest. It aims at a 
deposit of silver within the tubules and in such fine canals, filling 
them with a mirrorlike deposit. Howe's claim of canal sterility is 
endorsed by Price and Brooks. 

1 Dental Cosmos, November, 1895. 



47S REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

Two solutions are used: 

Solution A. 

Silver nitrate 3 grammes. 

Water 1 m ii. 

Aqua ammoniae fortior 2.5 c.c. 

The silver nitrate is first dissolved in the water and the ammonia 
added gradually till a black precipitate is formed and redissolved. 

Solution B. 

Liquor formaldehydi (formalin) 1 part. 

Water 3 parts. 

Making a 10 per cent, solution. 

Fig. 472 Fig. 473 





Showing it to be possible to use this Illustrating the manner in which the 

method in anterior teeth. No discolora- solution finds its way to the very end of 
tion of crown. (Howe.) the root, even when the broach is unable 

to reach it. (Howe.) 

The interior of the cavity and pulp cavity is coated with sticky 
wax (or a cavity varnish) . This is perforated with a cold, wet instru- 
ment. Solution A is run in with a smooth broach, gently raised and 
lowered. A drop of Solution B is added and run in allowing a few 
minutes. This is absorbed and the process repeated three times. 
The canal is then dried by absorption and Solution A is applied 
alone to remove all formaldehyd. This is followed by eugenol, 
which in recent extirpations is dried out and the canal filled. (Howe 
employs aristol zinc oxid and eugenol paste with a gutta-percha cone.) 



THE FILLING OF ROOT CANALS 479 

In septic cases the eugenol is sealed in and the process repeated 
at a second sitting at which the canal is filled. (See Figs. 472 
and 473.) 

Root Canals in Temporary Teeth. — The difficulty in temporary 
molars which are the ones usually treated is their resorbed root ends. 
Probably paraffin and aristol or Prinz's paraffin root filling meets the 
indication best, as a resorbable material is desirable. 

Buckley recommends in cases of chronic abscess the use of a stiff 
mixture of calcium phosphate and formocresol (formalin, 1 part; 
cresol, 2 parts), to be packed into the pulp cavity and zinc phosphate 
flowed over it. 

Johnson recommends euca-percha to be pumped into the canals 
and pressure with temporary stopping to be exerted until the solution 
appears at the fistula. Such temporary stopping as does not interfere 
with filling integrity should be left. 

Root Canal Filling Coverings. — Having radiographed the root to 
ascertain if the filling is satisfactory, the covering may consist of 
temporary stopping plus a trifle of thymol or oxychlorid of zinc to 
prevent infection and discoloration. This may occupy the pulp 
chamber unless anchorage therein is necessary. 

Pulp Digestion. — Harlan recommended that the following paste be 
applied to unremoved portions of dead pulps as a means of digesting 
them preparatory to root filling : 

]$ — Papain gr. v 

Price's pure glycerin lUiv 

Sol. 1 to 200 hydrochloric acid lUv— M. 

This is applied in the pulp canal, covered with blotting paper 
soaked in liquid vaselin, and the whole temporarily sealed for a few 
days. The pulp is reduced to the consistence of jelly and can be 
readily washed out. It might be of use in an impasse. 

The Filling of Perforations. — Perforations made high up in the canal, 
after being appropriately sterilized with formocresol, should be filled 
with gutta-percha cones and chloro-percha, and the apex amputated. 

In low perforations without a fistula associated, the opening of 
the perforations should be enlarged inwardly and a ball or plaque of 
aseptic, warm, low-heat gutta-percha, or even temporary stopping, 
adapted to the opening. A piece of pure gold plate may be burnished 
over an accessible opening, and be adapted with thick chloro-percha 
or temporary stopping. Any of these may be fixed in place with 
oxyphosphate of zinc. Quick-setting oxyphosphate of copper in its 
soft, gummy, state may be painted over the tissue and root opening 
by means of an instrument, or the perforation may often be satis- 
factorily closed with copper amalgam. When in posterior teeth a 



480 REMOVAL OF DENTAL PULP AND ROOT-CANAL FILLING 

pin must be used, the pin may be made smaller than the root canal 
and be coated with wax, soft oxyphosphate of copper is put in the 
canal, and the pin gently thrust in. When the cement has set the 
pin may be heated and withdrawn, and when included in the intended 
superstructure, the pin may be again cemented in place (see Figs. 
325, and 328). 

When a perforation threatens to produce an abscess an artificial 
fistula should be made and the case treated accordingly. 

If a perforation have a fistula associated with it, the oxyphosphate 
of copper or zinc oxychlorid may be allowed to go through the fistula, 
by way of which any excess may be removed. In some accessible 
cases I have even used local anesthesia, cut down upon the perforation, 
packed the artificial fistula open, prepared as for a small filling and 
filled with amalgam, polishing on the following day. The tissue seems 
to heal over the filling. These suggestions are subject to radiographic 
findings both before and after filling and may in future prove inadvis- 
able. (See Granuloma, Chronic Abscess, etc.) 



CHAPTER XV. 
GANGRENE OF THE PULP. 

Gangrene signifies a form of necrosis of tissue en masse, which has 
been caused by interference with its circulation. Thus an entire toe, 
a large portion of leg, a tooth pulp dying through a cessation of nutri- 
tion due to circulatory disturbance is gangrenous at the moment of 
its complete death regardless of its subsequent mummification or 
putrefaction which are the two results. (Seepage 51.) 

In general the gangrene is either due (1) to arterial obstruction, 
e. g., thrombosis of the femoral artery causing ischemia of the leg 
and subsequent death from lack of nutrition, a condition only pos- 
sibly due in the pulp to apical obstruction by closure of the apical 
foramen or to embolism of the pulp artery (infarction) . In such case 
the part is dry, reasonably aseptic and generally mummifies. (2) To 
venous obstruction, producing profound venous hyperemia, nutrition 
ceasing after available food supply is exhausted; death resulting. This 
is the common condition found in spontaneous pulp death, owing 
to the anatomical peculiarity that the pulp is boxed in the pulp 
chamber and compression of the vein by the artery leads to venous 
hyperemia. (See page 392.) 

Though such a pulp usually putrefies, there may be a period as 
when a pulp dies by venous hyperemia from thermal shock, during 
which there is no infection. This is a true, pure moist gangrene, as 
the pulp is full of blood and fluid. 

There are other forms of pulp death possible, e. g., progressive 
ulceration, but the writer believes that whatever the irritant at the 
pulp bulb, chemical or mechanical irritation or infection producing 
inflammation, thermal shock inviting arterial blood (arterial hyper- 
emia), inflammation or hyperemia of apical tissue, causing a sec- 
ondary arterial hyperemia, or the irritation of arsenic, there is always 
first arterial hyperemia, followed by venous hyperemia in the remain- 
ing tissue before its death, en masse. That this may be but a partial 
venous hyperemia accounts for the persistent vitality in many cases. 
The pulp usually dies first at the bulb in nearly every case, but this 
is but the natural effect of stagnation of blood prevented from 
escaping, at least partly, from the somewhat compressed vein, while 
the enlarged artery compressing it brings an excess of blood. If the 
compression should be profound total death would rapidly ensue. 
31 (481 ) 



482 GANGRENE OF THE PULP 

As in every case of gangrenous pulp, the pulp tissue either dries 
into a shrivelled mass or putrefies, we have the conditions dry 
gangrene or pulp mummification and moist gangrene or pulp putre- 
faction; these being the terms employed by general pathologists. 

DRY GANGRENE OF THE PULP (PULP MUMMIFICATION). 

Definition. — By dry gangrene of the dental pulp is meant its death 
in toto and its subsequent transformation into a dry, shrivelled mass 
occupying the pulp chamber and canal. 

Causes and Pathology.— If the pulp die and remain under conditions 
which exclude bacteria from contact with it, the water of the pulp 
may be removed, leaving the organ as a tough, shrivelled mass (Fig. 
474). The conditions most favorable seem to 
Fig. 474 be: q) Pulp death from some aseptic cause, 

e. g., the hyperemia resulting from a blow on a 
sound tooth; (2) constriction of the apical fora- 
men, due to hypercementosis, the result of thread 
biting or other mild irritation of the pericemen- 
tum; (3) the presence of secondary dentin over 
the bulbar portion of the pulp, causing pulp ex- 
haustion yet protecting it from infection; (4) 
Dry gangrene of the the capping of the pulp with zinc oxychlorid or 
pulp: pn, pulp no- formagen paste, the pulp being permeated with 

dule; DP, shrivelled 5 F . ' Y *i. .1 • f 1 

pulp. (From a sped- the drug or dried by it; (5) the covering ol pulp 
men of pulp extracted stumps with a paste containing a tannif ying 

intact in this con- . , , „ i i 1 1 

dition.) substance, such as alum, formaldehyde, or 

tannin. 

The water necessary to putrefaction is abstracted, either naturally 
or chemically, and probably bacteria are at the same time excluded, 
either mechanically or because the chemical substances used have 
penetrated the pulp tissue, acting as antiseptics. 

Symptoms. — The tooth has a nearly normal color, but under a 
reflected light is seen to have lost perfect translucency. There is no 
response to thermal or electric tests for pulp vitality. The dentin is 
insensitive to cutting instruments, and the cuttings upon the bur 
have no odor. There is no odor or fluid in the pulp canal when this 
is entered, and the pulp is found as a tough, dry mass not unlike 
that seen in a dry extracted tooth which contained a vital pulp at 
the time of extraction. These cases as spontaneous occurrences are 
relatively rare. 

Treatment. — If septic matter be introduced a violent pericementitis 
may be lighted up; but if aseptic precautions be employed in opening 




DRY GANGRENE OF THE PULP 



483 



the canal, and this be kept under the influence of a germicide, such 
as 5 per cent, formaldehyde, the root may be filled. A dressing of 
modified formocresol may be introduced for a time and the root then 
filled. The case should be radiographed for possible apical granu- 
loma. No available record of a granuloma exists as these cases may 
very rarely be seen. 

A temporary filling of pink base-plate gutta-percha is to be inserted 
in the crown cavity until all irritation, if any, subsides. 

Slight aseptic apical irritation may be anticipated as a matter 
of precaution by the use of iodin as a counterirritant at the time 
of root filling (see page 391). Such irritation is either mechanical or 
due to the chemical substances used. 

Tests for Pulp Vitality.— The diagnosis of pulp vitality or death 
being in practice almost daily required, the tests are here indicated. 
Some of these are decisive when used and no other need be used. 
Again several tests may be needed. Even radiography is not always 
decisive. 



Fig. 475 



Fig. 476 





Two vital teeth so found on drilling 
(see text) . 



Vital bicuspid, showing non-septic 
pericementitis due to overwork (see 
text). 



1. Sensitivity of dentin upon cutting, touching a tooth neck, re- 
sponse to such remedies as absorb water — glycerin, potassium carbon- 
ate, zinc chlorid, etc. (see page 324), are evidences of vitality. Lack 
of response is not a final test of death, but must be supplemented by 
other tests. Thus a cavity may sometimes be nearly prepared with- 
out sensation, but on drilling a retention, a last-procedure sensation 
is produced. It is decisive if characteristic. Thus in Fig. 475 drilling 
toward a pulp in the bicuspid suspected of death established its 
vitality as did drilling through the crown on the molar. The molar 
crown was removed on suspicion of septic cement because of suspicion 
that it acted as a cause of systemic depression. Excavation for a 
filling on the side of the crowned bicuspid in Fig. 476 gave the same 
result. 



4S4 GANGRENE OF THE PULP 

2. A tooth containing a vital pulp is translucent and pink; that 
containing a dead one always opaque to transmitted light even when 
it looks normal to the eye, and usually clouded to a gray or bluish- 
black, though sometimes yellow or brown. The ordinary appearance 
by reflected light often corresponds to this, but sometimes a tooth is 
clouded by fillings, or looks dead, but is vital. In such case the 
cervix may show normal translucency. In one case of neuritis a 
search for de vital teeth was instituted. A molar with clouded cervix 
was suspected and electrical test proposed, but on casual exploration 
a sensitive neck was discovered. This being test No. 1 was decisive 
of vitality. 

An electric mouth lamp with or without a reflector so arranged as 
to reflect the light upon the lingual surface of the tooth will supply 
the means for this test. In its absence strong sunlight may be 
reflected by means of a mouth mirror, but is not nearly so good a 
means as the electric light (Fig. 309). 

3. A strong odor of putrefaction may be obtained from bur cuttings 
in cases of moist gangrene only. This must be differentiated from 
the odor of decayed dentin, which usually also has an acid character. 
In case of partial death of the pulp not discoverable by the test 
given above, a fine, sharp probe passed into contact with the pulp 
remnant will demonstrate its vitality or death. 

4. If the tooth be isolated by means of rubber dam and, first, cold 
water be thrown, or, later, ethyl or methyl chlorid be sprayed upon 
it or upon the filling contained in it, or a pointed bit of ice be applied 
to the tooth or a filling, absence of response will indicate either par- 
tial or total pulp death or the formation of a quantity of secondary 
dentin. In the latter case the test must be renewed as the excavation 
proceeds. Degeneration of the pulp may be thought of, but pulps 
need not be removed because of such suspicions unless other symptoms 
demand it. 

A burnisher heated in the flame or a gutta-percha heater (electric), 
or hot copper ball or hot gutta-percha applied to a filling or dentin, 
or very hot water thrown upon an isolated tooth, should provoke at 
least a delayed response from a vital pulp. 

This test is positive for vitality if the tooth responds vigorously, 
but should be coupled with other tests if no response is obtained. 
Isolation by dam or tilting back the head and testing first posteriorly 
then progressing forward, are the best means of localizing the test 
(see test for arterial hyperemia). 

5. The application of a small high frequency glass electrode (violet- 
ray; to the enamel of a vital tooth produces a peculiar sensation not 
unlike that of hypersensitive dentin. It is due to the fact that the 



DRY GANGRENE OF THE PULP 485 

enamel is like glass unable to insulate the high frequency current 
which passes to the dentinal fibril. A devitalized tooth will not 
respond. The facility of this test makes the apparatus a very valu- 
able time saver in anterior teeth. Jumping of the current from the 
side of the tube necessitates care in posterior teeth. It may confuse 
if it jumps to the gum. It is well to take up the current with the 
finger on the side of the tube at first and to raise the finger after the 
glass is in contact with the tooth. (See Uses of Electricity.) 

Fig. 477 




Faradic battery. The electrodes described in the text should be substituted for those 

shown. 

Woodward has shown that if a few cells of a cataphoric apparatus 
(also ionization apparatus) are in action and the positive electrode 
be applied to the dentin or metal filling in a vital tooth, while the 
negative pole is at the cheek or wrist of the patient, a distinct sensa- 
tion should be felt, while in case of a dead pulp there will be no 
response; usually even a small filling will transmit a distinct shock 
in a vital tooth which is absent in a devitalized tooth. A mild inter- 
rupted current was suggested by Marshall and is a valuable test. 
A helix or an ordinary Faradic battery may be used. The batteries 
bought serve a current that is satisfactory if applied to the enamel 
through which the shock may be felt, but is too strong if applied to 



486 GANGRENE OF THE PULP 

fillings or dentin. The test upon the tooth exterior is sometimes 
best, as when there is no filling or it extends to the gum which is a 
confusing factor, but sometimes it is difficult to get response, while 
a filling will allow it, though curiously one filling may permit the test 
while another may not. The electrode may be covered with wet 
cotton and carried to the enamel, about over the pulp being the best 
point for response. If desired to test via the filling, it is best to use 
an electrode containing water resistance. This is easily made by the 
use of a glass tube corked at either end. Through each cork is run 
a bit of brass or copper wire. One end is coiled to receive the ordinary 
electrode cord pin, the other is left plain. The tube is almost filled 
with plain water and the wires extend through the corks, with their 
interior ends approximating each other only. The closer the stronger 
the current due to lessened water resistance. With this electrode the 
most delicate or strongest possible current may be obtained. The 
delicate is needed for touching fillings or dentin. In use one electrode 
is held in the patient's hand, the other by the operator. The electric 
current is of no definite use with gold crowns unless an opening 
large enough to obviate conduction by the gold to the gum be made. 
Here the thermal test may cause response or on drilling sensation be 
secured. A mild current should always be used unless there is no 
response, when the strength of the current should be increased. It 
is generally possible to test some evidently vital tooth nearby as a 
control. If the filling reach the gum, the current may be transmitted 
by it. The possibility of contact of the filling with another in a vital 
tooth is to be remembered. Insulation with rubber dam is indicated 
even if only run between teeth. 

There are various grades of response even in similar fillings in the 
same mouth, equally worn dentin, cavities, etc. The writer doubts if 
any definite judgment may be obtained of the pathological conditions 
of a pulp that can be depended upon and not better indicated by other 
tests, though of course the more irritated the pulp the greater the 
response. Very feeble response may warrant entrance, but tests 
should be renewed as one proceeds and symptoms and other tests 
should confirm the diagnosis. Sharp response indicates vitality. 
When the filling goes to the gum and response is obtained, it is well to 
touch the gum alone to determine if the shock is the same. 

In a few cases with vital pulps no response has been obtained upon 
repeated tests and the vital pulp has been drilled into. Usually 
secondary dentin is the insulator probably not containing vital 
fibers when the test is negative. The test is valuable though assertion 
to the contrary has been made, but the writer believes no more than 
determination of vitality should be demanded of it. 



MOIST GANGRENE OF THE PULP 



487 



In doubtful cases, such as that shown in Fig. 478, radiograph is 
valuable, and indicates at least the removal of the filling for further 
diagnosis and treatment. A root filling or a granuloma are evidence 
of pulp death. It does not distinguish a dead pulp if dentin is still 
over the horn. 

The presence of a fistula near a discolored tooth is strong evi- 
dence of pulp death with apical abscess, but pericemental abscess on 
a vital tooth must be excluded by tests for vitality, etc., usually the 
devital condition of the tooth is evident by its color. If more than 
one tooth offers confusion one should explore the direction of the 
fistula or employ a radiograph. 



Fig. 478 



Fig. 479 





Moist gangrene. Radiograph of 
unfilled root canals with large mass 
of filling material built in over 
them. (Price. 1 ) 



Case showing apparent apical infec- 
tion. Pulp positively vital. 



Movement at the root apex on tapping a tooth, while a finger is 
placed over the apical region, indicates some bone disappearance there 
(Talbot), but the sign must only be held as corroborative evidence 
or as leading to suspicion of apical abscess, etc. 

In making observations and tests one looks for positive facts and 
reactions. If all are negative, carefully drilling out a filling, retesting, 
endeavoring to get some test reaction, especially sensitivity at one 
side, and response to thermal or electric test. With still no reaction 
one may advance continuously toward the pulp and even before 
exposure may obtain the signs desired. In a very few cases, all signs 
are negative and one must either drill to the pulp or let the pulp 
alone. 



MOIST GANGRENE OF THE PULP (PULP PUTREFACTION). 

Definition. — By moist gangrene of the pulp is meant death of pulp 
tissue en masse in a moist state (see page 481) and. by pulp putrefac- 
tion its subsequent decomposition by the action of putrefactive agencies. 

1 Items of Interest, 1901. 



48S GANGRENE OF THE PULP 

That moist gangrene may occur before putrefaction was shown on 
page 481. They are usually classed together. As putrefactive decom- 
position is the essential feature in these cases, and that which gives 
the process its pathological significance, the causes, nature, effects, 
and treatment of putrefactive decomposition of the pulp are included 
under this subheading. 

It may be partial, as when the bulb of a pulp only is dead or when 
the bulb and one canal filament is devitalized. It may be total. 

Causes.— The causes of moist gangrene are such as may cause the 
death of the pulp and its subsequent decomposition by bacteria. 
Without bacteria putrefaction cannot occur. Among these the Strep- 
toccus brevis (viridans) is prominent, but the Bacillus putrificus 
and Streptococcus viridans, especially the latter, have latterly been 
strongly urged as the cause. Sieberth, 1 using teeth with dead pulps 
not too closely exposed, found streptococci as the common organism, 
only occasionally contaminated by others. Goadby, Kantarowicz and 
Niedergesass found Streptococcus brevis (viridans) in deep layers of 
decalcified dentin, and as the Streptococcus brevis are the chief ones 
found in apical chronic abscess, Hartzell and Henrici argue that it is 
probably the sole organism causing non-purulent pulp death. Four 
types of cases are seen: (1) In teeth apparently sound; (2) in teeth 
filled, but the canals not treated — i. e., death of the pulp has occurred 
after filling; (3) in teeth filled with canals partly filled; (4) in teeth 
having open cavities and canals. 

In the first type of cases the bacteria may enter by way of the 
blood channels, but it is not improbable that slight cracks or histo- 
logical defects in the enamel may admit to the dentinal tubules the 
necessary bacteria, or that they may gain entrance by way of the 
cementum and dentin at the neck of the tooth. (See Caush's Tubes). 
The inference is similar in case of trimmed crowns of teeth underlying 
gold caps. The infection might occur by way of the gingival groove 
and pericementum, hematogenously which might per se, cause pulp 
inflammation and death or infect a pulp dead by other causes (see 
pyorrhoea) . 

Many of these teeth do not develop acute abscesses even after the 
tooth has become dark in color; granuloma may perhaps be present. 
If the dentin be exposed, as at the incisal edge, the abscess may 
develop. The entrance of air or beginning of treatment often starts 
an abscess unless antisepsis is instituted. 

The access of oxygen increases the virulence of the bacteria present, 
though in some cases others may be introduced. 

1 See Hartzell and Henrici: Jour. Nat. Dent. Assn., May, 1917. 



MOIST GANGRENE OF THE PULP 



489 



Pigment. 



Fig. 480 
Sulphur + hemoglobin. 



In the filled cases crevices about the crown and root fillings may 
admit bacteria, which may pass through the spaces in even secondary 
dentin in some amount. On the other hand, it is irrational not to 
admit the possibility of an infection via the circulation (for example 
from another focus of infection). 

In cases of obvious pulp infection beneath fillings — e. g., suppura- 
tion of the pulp — the bacteria necessary are in situ. 

In the open cases the infection 
obviously arises from the mouth 
and a varied infection may result. 

Pathology and Morbid Anatomy. 
— The pulp being wholly or partly 
dead from any cause whatever, 
saprophytic bacteria gain access 
to it, if not already present, and 
the serial decomposition it under- 
goes is in exact correspondence 
with that of moist gangrene or 
putrefaction in other localities. 
In this serial decomposition albu- 
minous substances are first trans- 
formed into peptones and allied 
substances, some of them being 
very toxic. Compound ammon- 
ias, known as ptomains, or animal 
alkaloids, such as putrescin, 
neuridin, and cadaverin, are 
probably 'next formed. Next the 
nitrogenous bases — leucin, tyrosin 
(amido-acid), and the amines 
(methyl, ethyl, and propyl) — 
make their appearance, together 
with organic fatty acids, Next 
aromatic products, indol, phenol, 

cresol, etc., and finally hydrogen sulphid, ammonia sulphid, carbon 
dioxid, and water. By alternating processes of hydration, reduc- 
tion, and oxidation, bodies of increasing simplicity of chemical 
composition are formed. "Fermentation and putrefaction can only 
occur where the fungi concerned live." The contents of the tubules 
(fibrillse) also are putrefied. These products are derived from the 
following chemical constituents found in normal pulps, according 
to Hodgen: Proteins and albuminoid, fibrin, hemoglobin, collagen, 
elastin, fats, tripalmitin, stearin, and olein. 




C0 2l NH 3 ; 
H 2 and H 3 S. 



Aromatic and 
fatty prod- 
ucts. 

Ptomains. 



Peptones. 



Diagram illustrating the more com- 
plete decomposition of the pulp at its 
coronal end. 



490 GANGRENE OF THE PULP 

The irritant bodies are probably the gases and ptomains which 
have experimentally been found capable of producing suppuration in 
the absence of bacteria. The bacteria are also irritant. 

The hydrogen sulphid combines with the HN 3 of proteid origin, 
to form ammonium sulphid (NH^S, which, again, combines with 
the iron in the hemoglobin of the red corpuscles, producing ferrous 
sulphid, Fe2S, which darkens the decomposing tissue, and, entering 
the tubules, stains the dentin a slate-gray or bluish-black color. 
Other derivatives of hemoglobin may be responsible for the yellowish 
brown discoloration often seen in cases in which bacteria have not 
reached the pulp until long after pulp death. The color is,, therefore, 
not due to the presence of hydrogen sulphid. 

Miller 1 found that the reaction in cases of putrefaction was alkaline 
unless a certain percentage of sugar was introduced into the medium, 
when it was acid. He explains the voluminous foul odor of confined 
dead pulps as due to the absence of oxygen of air. If present as in 
open pulp cavities the gases escape, the volume being therefore 
reduced, oxidation of gases increased, and an acid reaction due to 
entering carbohydrate permitted. The exact nature of pulp decom- 
position is in some doubt. 

Fig. 480 is a diagram illustrating these changes; it being assumed 
that the decomposition is most advanced at the crown portion of the 
pulp, owing to the entrance of bacteria at that point. 

In the early stage of the process the gangrenous pulp resembles 
a yellowish mass of sloughing tissue, with reasonably tough con- 
sistence, which can be easily removed. In the later stages it is more 
decomposed and dark and jelly-like, and yields to the broach. 
Naturally the greatest number of fungi will have, by multiplication, 
invaded and putrefied that end nearest the source of infection, while 
the more consistent (less putrefied) portion of the pulp will exist 
at the apex. In the final stages nothing but fluid; or even an almost 
dry canal, may be found. This last condition must not be con- 
founded with dry gangrene. If fluid, or odor without fluid (gases), 
be present the case is one of moist gangrene. 

Gangrenous pulps do not necessarily produce abscesses at once, 
but often clinical history shows that a year or two, or even more, 
may elapse; the possibility of granuloma as an intermediate step 
being admitted; though as short a time as two or three weeks has 
sometimes been sufficient. In one case of a boy, aged ten years, the 
time between a capping of a bleeding pulp with Jodoformagen and 
the presence of a fistula upon the gum was but two weeks. It was, 

1 Microorganism of the Human Mouth, 1890. 



MOIST GANGRENE OF THE PULP 491 

however, in a temporary first molar, and the cement covering the 
cap was found to be loose. 

The forcing of gangrenous pulp tissue by instrumentation into 
apical tissue generally results in an abscess, even when extraneous 
bacteria are presumably not introduced. 

The irritating substances in a decomposing pulp are presumably 
the bacteria, the ptomains, and the expanding gases. 

Many decomposed pulps produce no pain, but in these cases 
the gases may escape via dentinal tubules and leaks about fillings 
(Fig. 478) or the condition of granuloma is established, owing to the 
Streptococcus viridans type of infection. 

Clinically, putrefactive pulps may be found in sound teeth, in 
filled teeth, and in teeth the pulp cavities of which are open to the 
oral fluids, either actually or through the medium of open tubules 
in the dentin over them, or in apical portions of poorly cleansed or 
partly filled canals. A cotton dressing having a bad odor, or an 
apparently empty apical portion of canal or a leaky gutta-percha 
canal filling associated with a bad odor, even though the pulp has 
been successfully removed, have a similar pathology. There is 
little difference in principle between putrefactive serum or tubule 
contents and a putrefactive pulp. Any of these may cause abscess 
or remain quiescent. There may be apical granuloma, 'but in many 
cases there is no evidence in the radiograph. 

Symptoms. — The symptoms are opacity of the tooth evident to 
the eye or noted by transmitted light, bluish or brownish discolora- 
tion of varying degrees, odor, and discoloration of the dentin in a 
cavity. 

There is a lack of response to tests for vitality (see page 483). 
Sometimes a bad taste due to leakage about fillings is present. Upon 
drilling out a filling the odor of putrefaction may be clearly noticed 
even before entrance of the canal, and sometimes rises to the operator's 
nostrils. The odor of the bur cuttings is diagnostic in less pronounced 
cases. The gases may be present in quantity without symptoms of 
pain. Looseness, tenderness to percussion, incipient and acute 
abscess, or a chronic fistula are evidences of pericemental irritation. 
Granuloma or partial root filling noted by radiography is corrobora- 
tive evidence (see page 487). 

Pain to heat, while usually indicative of pulp irritation, also some- 
times occurs, and is explainable upon the same theory of the expan- 
sion of gases against vital tissue — in this case the apical tissue — 
though sometimes a pulp remnant is present. These symptoms 
are all explained by the pathology of the condition. 

A confusing condition clinically is found where one-half of a pulp 



492 GANGRENE OF THE PULP 

has died and undergone decomposition, as in molars, the other half 
remaining vital, although the seat of infection and inflammatory 
action. So far may this condition go, that abscess, acute or chronic, 
may be present upon the root of one tooth long before the second 
segment of the pulp has succumbed. The diagnosis is usually one 
of pulp putrefaction, perhaps rendered doubtful, by a response to the 
thermal changes or electrical tests, which doubt can only be cleared 
up by finding the dead and ulcerated portions. 

In one case of a lower molar with a fistula related with the distal 
root I found the pulp apparently vital upon entering the pulp chamber 
with a bur at a point about midway between the horns. There was 
apparently a persistence or hypertrophy of the pulp bulb attached to 
the mesial filaments. The distal canal was found to contain only the 
fluid remains of a dead pulp filament. In cases seen at the right 
time the bulbal half of a pulp may be gangrenous with or without 
positive putrefaction, while the apical half is still vital. 

J. H. McQuillen 1 recorded a case of longitudinal fracture of a 
bicuspid tooth extending from the sulcus to the bifurcation of the 
roots, and which was apparently due to the expansion of the gases 
of decomposition. Poinsot 2 records a similar case, and states that 
several teeth containing decomposed pulps confined in a glass tube 
caused the latter to break. 

Fig. 481 




Tooth split by gas. (Roff.) 

Dr. S. H. Roff, 3 of Cincinnati, Ohio, has presented the case shown 
in Fig. 481. He had it under observation for seven years. He 
regarded the case as one of slow progressive cracking (a run) with 
final irritation and death of the pulp and the final clean longitudinal 
fracture as due to the gases from the partially decomposed pulp. 
When one considers the fact that wet plugs of soft wood will split 
granite boulders we must accept the possibility of tooth fracture 
by gas pressure. 

i Dental Cosmos, 1871. 2 Ibid., 1901. 

3 Items of Interest, March, 1912. 



MOIST GANGRENE OF THE PULP 493 

Observations previous to that of McQuillen have recorded a sound, 
as of an explosion, to have occurred simultaneously with the fracture 
of the tooth. I have looked all my professional life for such a case, 
but though I have seen quite a number of clean fractures I have 
never been able to eliminate the possibility of fracture from ordinary 
causes and in some of the cases have had positive histories of direct 
violence. Peculiar fractures of roots are shown under the caption of 
Mechanical Injury. The cases in Figs. 246 and 249 may have been 
due to gas as there was no history of violence and the crowns were 
intact except for a large filling in one case and a crown in the other. 

The direct result of partial pulp putrefaction, whether as a result 
of gangrene or suppuration, is inflammation of the remainder of the 
pulp; when there is no remainder, inflammation of the apical tissue. 
The first result of apical irritation may be either acute abscess or far 
more commonly, a chronic proliferative inflammation known as 
granuloma, which frequently having no symptoms, should be sus- 
pected in every case and its presence or absence determined by 
radiography. This condition is to be later considered. 

Treatment. — The pulp being presumably infected, all quiescent 
gangrenous pulps or putrefactive conditions under any conditions 
discovered indicate a similar treatment, namely, first disinfection to 
remove or kill bacteria w T hich might cause an abscess and at the 
same time to destroy the chemical nature of the gases and ptomains. 
After this the canals are to be thoroughly opened, cleansed, further 
disinfected for the sake of surety, and later filled; granting granu- 
loma or chronic apical abscess to be possibly present the added 
responsibility is merely to prevent introducing into an abnormal tissue 
bacteria which may cause an acute abscess and to destroy such bac- 
teria as may be there present without such injury to the soft tissue as 
may prevent regeneration of sterile tissue. 

The profession is largely in doubt regarding the actual value of the 
medicaments used in canals as sterilizing agents. Brooks and Price, 1 
following the general method laid down by Dahlgren, 2 practically 
eliminated all remedies as agents capable of disinfecting canals with 
100 per cent, efficiency, with the exception of dichloramin-T in 15 
per cent, solution in eucalyptol, and chlorazen, in 4 per cent, aqueous 
solution, in six daily treatments, both considered too painful and 
destructive for use, and Howe's ammoniated silver nitrate and forma- 
lin, which seemed to sterilize in about ten minutes, but was objec- 
tionable on account of the discoloration. 

^Journal of Nat. Dent. Assn., March, 1918. 
2 Ibid., 1917. 



494 GANGRENE OF THE PULP 

Howe 1 introduced the above method of disinfection of root canals 
and tnbuli and inaccessible root ends, which has received the en- 
dorsement of Price and Brooks 2 working in the Research Laboratory 
of the N. D. A. (Described on page 477.) 

Howe uses occasionally a rubber pellet to force the solution into 
the canal and abscess tract if such exist. 

For final treatment the canals are filled with a paste of zinc oxid 
and eugenol plus aristol, into which is thrust a gutta-percha point. 

Howe claims immediate sterilization even in cases of aborted acute 
abscesses, not only of the canal, but of abscess tracts (and fistulae), 
with allayed irritation rather than irritation from the treatment. 

The method offers much hope for unexplorable root ends in cases 
of both recently removed pulps and septic cases. Howe claims canal 
sterility in all cases. Price and Brooks state, in confirmation, that 
sterilization seems likely in about ten minutes. The dam is preferably 
applied or the tissues otherwise protected. The hands should be 
protected with rubber gloves or finger cots. 

Prinz 3 claims that dichloramin-T in 5 per cent, solution in chlor- 
cosane (a heavy oil made from hard paraffin by replacing part of its 
hydrogen by chlorin) is tolerated by tissues and will sterilize a root 
canal (by test of the incubated scrapings with sterile cleansers) after 
about three applications. 

Unfortunately, he states that in removing the canal contents while 
using this medicament, if extreme care be not used to avoid forcing 
canal contents beyond the apex, an acute abscess will ensue. If the 
opening does not reach to the apical tissue at the first sitting, a dress- 
ing should be sealed in, but should not be sealed in if no attempt is 
made to remove the canal contents. 

This of necessity limits its use as a canal germicide to large open 
canals or those which can be reasonably opened under dichloramin-T 
or by other means, as a further means of sterilizing apical tissues. 

Dunham 4 states that when well mixed with septic material dichlora- 
min-T, 2 per cent, solution, disinfects in less than half a minute 

The dressings are to be applied on sterile paper canal points, the 
endeavor being to coat the canal and, if possible, apply it to the apical 
tissue. The technic of canal cleansing is with sterile broaches dipped 
into the dichloramin-T (in a separate medicament glass) and slowly 
worked into the canal, wiping the broaches on sterile cheesecloth or 
bibulous paper. For canals requiring enlargement, Prinz recom- 
mends preliminary opening with sulphuric acid and neutralizing this 

1 Dental Cosmos, September, 1917. 2 Jour. Nat. Dent. Assn., March, 1918. 

3 Dental Cosmos, December, 1918, p. 1078. 

4 See Prinz, Dental Cosmos, December, 1918, p. 1077, 



MOIST GANGRENE OF THE PULP 495 

with sodium dioxid, washing out, reasonably drying, leaving the 
natural moisture to assist in evolution of chlorin and dressing with 
dichloramin-T. He eites successful cases so treated, though from 
past experience with preliminary sulphuric acid opening as a primary 
step I would feel a need of caution in the procedure; however, if the 
facts are generally as stated, there can be no contention over the 
method. 

Buckley claims that one or two applications of formocresol (cresol 
and 37 per cent, aqueous formaldehyde solution equal parts) in the 
pulp cavity only will so sterilize or inhibit bacteria that the canal 
can be safely opened mechanically if asepsis be observed. 

Brooks and Price rate formocresol as a germicide at 93 per cent, 
efficiency in twenty-four-hour treatment with crown sealed and root 
apex open, 1 but there have been numerous instances in the writer's 
practice in which pus flows from apical tissue have been checked by its 
use. Likewise, after its use there is seldom any ill result in rather diffi- 
cult canal openings. Buckley, in his book, 2 illustrates good results follow- 
ing its use quite comparable to any I have seen illustrated. Although 
it has been claimed that formaldehyde produces the result of inducing 
a granuloma in time when applied to healthy tissue and Grove 3 has 
produced experimental evidence to show irritation of normal tissue, 
it does not follow that diseased tissue will be unfavorably affected 
nor even that somewhat irritated normal tissue may eventually be 
damaged provided asepsis be produced. Grove has experimentally 
shown that formocresol merely sealed in the pulp chamber will find 
its way to the apical tissue. He claims hardening of such tissue, 
To me this seems to rather set an advantage for formaldehyde gas. 
Our object is to so affect diseased tissue as to render it sterile, leaving 
to Nature the work of removing even dead aseptic tissue if necessary 
through aseptic absorption. In this connection the action of phago- 
cytes should be depended upon as a means to an end. 

From clinical evidence I am not satisfied that formocresol and its 
congeners is so irritant as supposed. I frequently find apical tissue 
showing sensitivity after several applications and in cases of ulcerated 
pulp filament have often found them vital after even pure formocresol 
has been sealed in the pulp chamber. The case shown in Figs. 4S2 
and 483 is offered as evidence as are Figs. 459 and 460. Following 
Price and Brooks it would seem that to attain the best results one 
should change the dressing every twenty-four hours until sterile. 

1 Deduced by the editors from their experiments in Jour. Nat. Dent. Assn., March, 
1918. 

2 Dental Materia Medica, Pharmacology and Therapeutics, 4th ed. 

3 Dental Cosmos, February, 1913. 



496 



GANGRENE OF THE PULP 



The only other valuable means of sterilization is the introduction 
of medicaments by means of the galvanic current called cataphoresis 
if the positive pole at the canal drives the electropositive medica- 
ment unchanged toward the negative pole in the hand causing it to 
penetrate apical tissue or anaphoresis if the negative pole at the canal 
drives an electronegative medicament unchanged toward the positive 
pole iii the hand or electrolytic medication if the medicament is 
decomposed into its elements some of the ions being electronegative 
appearing at the positive pole (anions) and the others being electro- 
positive appearing at the negative pole (cations). Of these the elec- 
trolytic medication is the more valuable, the ions being nascent, 
owing to the electrolytic dissociation and therefore more active. The 
most valuable ions are those of zinc, copper, iodin, and chlorin. 



Fig. 482 



Fig. 483 





Lower molar, showing marked 
granuloma on distal root. Mesial 
root denuded, but having remarkably 
little pus discharge. Condition of 
this root due to a longitudinal frac- 
ture discovered on extraction. 



Same case as Fig. 482 after six 
months. Roots purposely deluged 
with formocresol. Distal root con- 
tains a gummy iodoform paste (see 
page 476). Note marked improve- 
ment in granuloma on distal root. 
(Position unfortunately reversed.) 



Sturridge 1 recommends a positive zinc electrode and a 3 per cent, 
solution of zinc chlorid as an electrolytic in the canal to dissociate 
positive zinc ions which migrate into the tissues and chlorin which 
remains at the positive pole, though it may slowly diffuse from that 
point as new ions are formed, or a positive copper electrode and a 
2 per cent, solution of copper sulphate to cause the migration of copper 
ions or iodin in the form of tincture (a solution) with a negative pole 
at the canal. 

Prinz 2 recommends a positive iridioplatinum electrode at the canal 
and a 1 per cent, sodium chlorid solution as electrolyte to pro- 
duce chlorin, which being electronegative forms about the positive 
electrode. This will not migrateinto the tissues unless formed in 
contact with them, but in the canals will produce surface sterilization 



1 Dental Electro-Therapeutics, p. 252. 

2 Dental Cosmos, April, 1917. 



MOIST GANGRENE OF THE PULP 497 

if employed for as many minutes as are equal to a quotient produced 
by dividing the constant figure 30 by the milliampere reading of the 
milliampere meter, for example, if a current of 3 ma. is passing ten 
minutes are required, if 2 ma., fifteen minutes. 

The cataphoric outfit being the same as the so-called ionization 
outfit, page 327 and the Chapter on Uses of Electricity are 
referred to. 

It is evident that the best use of electrolytic medication is in cases 
of ready access to at least apical portions of canals so that the method 
fails to reasonably apply to the early sterilization of fine canals. 

In an endeavor to correlate for the purposes of treatment of pulp 
putrefaction, I believe the following methods to be good practice, time 
being a factor secondary to results and avoidance of injury : 

1. In teeth in which eventual discoloration would not much matter 
and canals liable to be difficult, the employment of Howe's silver 
nitrate and formalin treatment for a first sitting. Thorough opening 
with acid, etc., the same being neutralized and the repetition of the 
Howe treatment at the second sitting. A repetition of the Howe 
treatment and root filling at the third sitting (see page 477). 

2. In teeth liable to afford access to root apices the placement of 
formocresol, geranium formol or 5 per cent, aqueous formaldehyde 
solution in the pulp cavity only for the first or first two sittings to 
avoid apical infections. Thorough mechanical cleansing at the second 
or third sitting, this to be followed by dichloramin-T, 5 per cent, in 
chlorcosane as recommended by Prinz. Repetition at the fourth and 
fifth sittings or the use of Prinz's technic throughout (see page 494). 

3. In apparently fine canals it may be best to apply formocresol, 
etc,, to the pulp chamber once or twice, later open with acids, etc. 
(see pages 443 and 465), and apply the Howe treatment as indicated. 

4. In case of granuloma, the Howe treatment may give results in 
inoperable root apices. This is as yet an unknown factor. If possible 
after disinfection in operable roots an opening should be made with 
broaches through the root apex. 

Thereafter phenolsulphonic acid (Buckley) or 5 per cent. dichlora- 
min-T (Prinz) may gently be introduced into the granulomatous area 
to sterilize and stimulate new growth or modified formocresol, etc., may 
be sealed in the canals, or the area may be treated electrolytically by 
means of a copper point and 2 per cent, copper sulphate introduced 
into the apical tissue and used as the positive electrode (furnishes 
copper ions), or the canal may be filled with zinc chlorid, 3 per cent, 
and a positive zinc electrode used to pass 5 ma. of current for about 
eight minutes (Sturridge) to either stimulate or disinfect the tissues. 
Or sodium chlorid solution may be the electrolyte, a positive plati- 
32 



49S GANGRENE OF THE PULP 

num point in the canal to liberate chlorin and sodium ions (Prinz) . 
Sturridge 1 has pointed out that this is a reversal of the proper poles. 

When formaldehyde is relied upon the first treatment consists in 
opening the pulp cavity and gently removing only the bulk of decom- 
posed pulp from the pulp chamber and canals, care being employed to 
avoid forcing any putrid material into the apical tissue by broaching or 
plunging of the bur. Also, no bacteria should be introduced from out- 
side. This involves the use of rubber dam and asepsis, all of which are 
discussed on page 448. Too much advance should not be made, the 
first object being sterilization. The opening should not be too freely 
made, and should be funnelled or countersunk outwardly to secure 
the seal against being plunged into the pulp cavity in mastication 
(Fig. 484). 

This being done, the canals .are dried with cotton and hot air, and 
a small pellet of cotton saturated with formocresol or 10 per cent, 
aqueous formaldehyde solution, or geranium formol 2 is to be placed 
in the pulp chamber. 

1$ — Formaldehyd 40 parts 

Essence of geranium, distilled 20 parts 

Alcohol 80 per cent 40 parts 

Any that has come in contact with the orifice should be removed 
with alcohol. The orifice is then dried and a small piece of dry spunk 
placed over the application, but not so as to interfere with the 
seal. Quick-setting, adhesive, hydraulic cement is now flowed into 
the orifice, air bubbles being avoided by flowing it in with an instru- 
ment (Fig. 484). A bit of paraform accomplishes the same purpose 
as the solution, namely, the liberation of formaldehyd gas. 

When opportunity for self -relief seems proper, as when the operator 
is leaving his practice for a short time, or may otherwise be inacces- 
sible, hot temporary stopping may be used and the patient instructed 
as to the proper procedure to obtain relief. An ordinary pin crooked 
at the point by striking it across any hard surface will serve to pick 
out the stopping and cotton. In all cases tight coverings must be 
made, as the object is to concentrate the action of the formaldehyd 
gas upon the canal and tubular contents. 

In some cavities it is well to make the covering first, as done for 
arsenic (see Fig. 391), and to seal the dressing in with a further 
addition of cement or temporary stopping. The latter does not 
permit mastication like the former. 

If there be a broad cavity extending beneath the gum, it is well 
to press the gum away with cotton pellets, then to form the cavity 

1 Dental Cosmos, 1919. 

2 Geranium-formol introduced by Andre and de Marion, l'Odontologie; abstract 
by International Dental Journal, 1901. 



MOIST GANGRENE OF THE PULP 



499 



and open the canal orifices. Then a retention at the cervical portion 
of the cavity should be made, even if it be necessary to drill a series 
of pits along it with a No. 1 bur. Spunk is now placed over the 
pulp canals and quick-setting amalgam is to be permanently built 
in at this part of the cavity. When set the spunk is withdrawn, 
formocresol in cotton is placed instead of the spunk, and the covering 
completed with cement. The amalgam is finished as far as practi- 
cable at the one sitting, and the case dismissed. At future sittings 
the rubber dam may be applied and the canal work done (Fig. 485). 
When cavity walls are frail, spunk may be placed in the pulp cavity, 
and a permanent cement lining built into the cavity. This can be 
perforated to the spunk, thus leaving the walls supported during 
the treatment. (See Figs. 515 and 516.) 



Fig. 484 



Fig. 485 





a, cotton and formocresol; b, spunk; 
c, cement. 



Cervical wall built up with amal- 
gam to permit canal sterilization 
and treatment. 



Formocresol, introduced by Buckley, consists of equal parts of 37 
per cent, aqueous formaldehyd solution and cresol, which combine 
well. 

According to Buckley, the formaldehyd not only acts as a germi- 
cide, but combines with the ammonia of ammonium sulphid to form 
urotropin and water, 6CH 2 + 4NH 3 = (CH 2 ) 6 N 4 + 6H 2 0, and 
with hydrogen sulphid to form sulphur and methyl alcohol, 2CH 2 + 
2H 2 S = S 2 + 2CH 3 OH. The cresol is supposed to act upon the 
fatty compounds, changing them into a compound resembling lysol. 
Thus, antiseptic substances are formed from poisonous ones. This 
does not necessarily represent all the reactions occurring, as many 
other compounds may result from putrefaction. The probability is 
that the thoroughly bactericidal action is the one of greatest value. 
This action has been shown by Mayrhofer to be true only for the 
first twenty-four hours; thereafter the bacteria in the tubules may 
grow back into the canal and the dressing, in spite of the fact that 
the odor of the dressing is present. The canal should therefore be 
mechanically cleaned after twenty-four hours, and a fresh application 



500 GANGRENE OF THE PULP 

be made. 1 Mayrhofer claimed inability to sterilize permanently 
with formocresol. Nevertheless the editor treats such cases at wide 
intervals ordinarily with impunity. In a few cases an abscess has 
supervened after the first dressing, but none as yet after the second. 
Leakage of the formaldehyd gas may have been the reason, but a 
chronic apical abscess has been a suspicion. Cleansing and reaming 
the canals at the first sitting is another danger, even when formal- 
dehyd is subsequently used. This must sometimes be done as when 
a crown is broken away and the root canal is foul. 

Formaldehyd is so efficacious in my hands that it has until recently 
displaced other methods in my practice and I use it despite the general 
trend against it, though occasionally some one publicly or privately 
praises it. While this is true for a great majority of the cases, occa- 
sionally a patient is met with whose tissues do not tolerate formal- 
dehyd well. In such a case if the foramen be open as is usual in such 
cases, any of the mild proprietary antiseptic washes as Listerine, 
Borine or Lavoris, Vernas lotion (astringents), with a trifle of iodo- 
form picked up on the dressing seems to accomplish the work if 
promptly renewed. Weak ammonia water has been occasionally used 
to counteract the formalin. 

When one pulp filament is gangrenous and another vital, the treat- 
ment is the same,, it being the writer's experience that formocresol 
loosely placed is not incompatible with ulcerated pulps, and, indeed, 
is an excellent dressing for suppurative pulps when modified to a 3 
to 5 per cent, strength; even full strength has been acceptably used. 
Later, the vital portion is appropriately removed. 

When root fillings are present in part of a canal they must be 
removed in order to treat the balance of the canal. 

The case is thus resolved into one of moist gangrene and treated 
accordingly. 

Wax may be removed by overheating with the hot root drier and 
absorption with cotton, or oil of cajeput may be used as a solvent. 
Paraffin may be removed in like manner, xylol is a solvent. 

If a cotton root filling be found it sometimes allows the broach to 
tear loose. In such case a Kerr broach is driven into it to create 
a central opening, after which the fibers become engaged by the 
barbed broach, though sometimes it must be drilled out. 

Chloroform, xylol, oil of cajeput or eucalyptol may be used to 
soften gutta-percha root canal fillings, and at times the smallest 
Kerr or Downie broach is to be bibevelled at its ends and used as a 
drill, cutting its way. This is very dangerous as perforations occur 

1 Viulleumier: Items of Interest, March, 1910. 



MOIST GANGRENE OF THE PULP 501 

if one deviate from the gutta-percha. Gutta-percha hardens in time, 
but still cuts more readily with xylol, etc., than root structure. When- 
ever one has to bore hard a radiograph with wire is advisable. Even 
this may confuse as showing a wire in good line with the canal mesio- 
distally from which one may still diverge buccolingually. In one case 
even after such a wire diagnosis I failed to find a canal in a lateral 
after two hours' search in various directions (Fig. 514). Oxychlorid 
and other cement fillings may have 50 per cent, sulphuric acid or 
strong ammonia water applied to them to assist in breaking up the 
bond of the cement by chemically destroying either the zinc oxid or 
the acid. The drill will tamp the fluid into the cement and cut the 
cement at the same time. 

All root fillings of cement nature are apt to be faulty when used 
as such, because the air in the canal prevents ingress. This fact is of 
importance in diagnosis in filled teeth, giving evidence of chronic 
pericementitis, i. e., there is probably an unfilled portion of root 
canal containing putrefied pulp or serum. One always seeks to drop 
freely into a canal lumen beyond the root filling. In doing this one 
is liable to compress the air or fluid in the apical region of the canal 
thus producing sensation and it is advisable to stop and reapply 
disinfectants at least before immediately proceeding with the work. 



Fig 




Little Giant post-puller. 

To remove pins from roots a bibevelled Kerr broach may be driven 
into the cement or dentin about it and the drifts united. The pin 
may often be forced to one side and then jigged loose. If there be 
sufficient pin extending above the face of the root a "pin puller" 
such as the "Little Giant" (Fig. 486) may be used. The S. S. White 
Dental Manufacturing Company makes one which extracts a pin 
broken at or below the level of the root face after trephining and 
threading the pin (Fig. 487). If the pin cannot be loosened it must be 
drilled out bodily. A sharp round bur should be used to countersink 
the end of the pin, and then by the aid of oil it is cut into shavings. 
Frequent desiccation and examination to observe the presence of a 
metal remnant is necessary to avoid the accident of perforation. For 
removal of a plain bandless dowel crown, Johnson's crown remover 



502 



GANGRENE OF THE PULP 



may be tried. In case of a banded dowel crown one must drill 
through the backing, separate the pin from the crown — remove 
the crown with forceps if necessary but with care may retain it 




S. S. White post-puller. 
Fig. 488 




Johnson crown remover. (Courtesy of Goldsmith Bros.) 
Fig. 489 




Medicament glass for holding broaches in sterilizing solution, etc. (S. S. White.) 



MOIST GANGRENE OF THE PULP 503 

for insertion of a new dowel the old one being removed as previously 
described. Sometimes crowns must be destroyed. If chloro-percha 
has been used in the setting (see page 509) this work may be avoided. 
Shell crowns may often be perforated for a "tap" into the root but 
if poor, should be removed. 

When for any reason one must work on a canal immediately, one 
may either proceed, as in the Howe method, allowing ten minutes for 
canal sterilization or in anterior teeth use the following: 

A little dry sodium dioxid is placed upon a slab with a drop of 
water near .it. A broach is drawn through the water, then through 
the powder, and the adherent powder carried to the canal and gently 
passed into the moist putrid contents of the canal; a reaction occurs 
between the water and sodium dioxid as follows: Na 2 2 + 2H 2 = 
H 2 2 + 2NaOH, producing hydrogen dioxid and sodium hydrate. 

The sodium hydrate or lye saponifies all fatty matters and destroys 
organic matter, even living matter, and the hydrogen dioxid liber- 
ates nascent oxygen, which is a disinfectant. No oil or phenol 
should be used with dry sodium dioxid, as an explosion may occur. 
The use of the alloy kalium-natrium in a moist canal causes a dis- 
ruption of the water molecules with production of flame by ignition 
of part of the hydrogen and of sodium and potassium hydrate by 
addition of (OH) to each metal making Na(OH) and K(OH). 

The result of the reaction should be washed out with a gentle 
stream of warm water, while a broach is gently passed to and fro 
through the mass. The action is then repeated as far as it can be 
carried. 

The danger in the use of these materials lies in the possibility of 
the production of a chemical inflammation of the apical tissue, due 
to the nascent hydrates, if the foramen be open, which inflammation 
may be severe. This is only to enable one to get a canal ready for 
sterilization of the tubuli and apical region, one must then proceed 
to accomplish this as indicated on page 493, etc. 

The withdrawal of all cotton dressings should be done under aseptic 
precautions, and repeated as indicated on page 497. As this procedure 
must be repeated to obtain sterility it should be done as often as 
required. This based upon the germicidal value of the medicament. 
To me there seems little practical value in a laboratory test of canal 
sterility. If one w r ait on a test the canal may become infected mean- 
while. If it seems sterile there can be no assurance of tubule or apical 
sterility and in fine apices one cannot test the most important areas. 
The apical granuloma cannot be accurately tested. 

Active hemorrhage may ensue or serum may ooze from the apical 
tissue. This may be checked with 25 per cent, pyrozone, adrenalin 



504 GANGRENE OF THE PULP 

chlorid, 1 to 1000, or, preferably, deliquescent zinc chlorid or alum and 
thymol, and the medicaments renewed. Particularly such as a mild 
antiseptic astringent and iodoform (see page 500). 

If the apical foramen be a large one, and if a pus flow follow the 
removal of the temporary dressing and be but slight, it should be 
absorbed and medicaments renewed. This is apical abscess. No 
such thing as immediate root filling is now T admissible nor will be 
until a permanently germicidal root canal, filling shall be found. 
Sometimes a thick, glairy fluid will ooze from the apical tissue. This 
is coagulable lymph, and the parts require treatment in the same 
manner. 

In order to prevent apical irritation in so far as possible, the gum 
is to be painted with ordinary tincture of iodin or spotted with the 
dental tincture of iodin, both lingually and buccally, as a counter- 
irritant. 

ty — Iodin 3iij 

Alcohol gj 

Shake frequently for a week or two. (Flagg.) 

If infection of the apical tissue by any chance ensue, either as the 
result of the operation of canal cleansing or previous to operative 
interference, the disease known as septic apical pericementitis is 
established. 

Pericementitis following the opening of teeth containing gangrenous 
pulps has been explained upon the ground that the bacteria in the 
absence of free admission of oxygen have lost their virulence, which 
is restored when the air is admitted. It is quite likely that either 
this is true or that extraneous bacteria are introduced during the 
course of treatment. 

In drying with the compressed-air syringe, care should be employed 
to avoid extensive emphysema of the cheek, which may be induced 
by intense pressure. If it occur, the emphysema should be reduced 
by manipulation, with a view to gently forcing the air back through 
the root. Christensen 1 and L. Greenbaum have each reported a 
case, and the editor had his first case when desiccating an accidental 
lateral perforation. This occurred even without close application 
of the syringe nozzle, 35 pounds pressure being used. 

Another case occurred while an upper lateral with large apical 
foramen and even with an open fistula was being dried out. The 
entire right cheek and lower eyelid was instantly puffed up. The 
patient called attention to a stiffness and coldness. It subsided 
upon manipulation. There might be dangerous sequelae if sepsis were 

1 Dental Cosmos, 1904, p. 151. 



MOIST GANGRENE OF THE PULP 505 

present. This applies more particularly to cases with large foramina 
or perforations as above noted, but care should be employed. A hot 
point electric drier used repeatedly or an Evans's root drier (Fig. 393) 
are more valuable for the apical ends of roots, as the air seldom 
reaches that point. Moreover, air should be filtered before passing 
through the compressor. Cotton twists and paper points used for 
drying must be sterilized before use. (See Asepsis.) 

In a few cases the continuity of the canal has been lost because it 
has become involved in caries upon one side of the root. This may 
be treated as described on page 354. 

Discoloration of the Teeth by Moist Gangrene. — In the final decom- 
position of the pulp a pigment molecule is formed, which, entering 
the tubules or formed in it, stains the dentin and imparts an abnormal 
color to a portion or nearly all of the crown, which ranges from 
an almost imperceptible loss of translucency to a yellow-brown, 
slate-gray, or bluish-black color. Also in conditions of venous 
hyperemia or pulpitis, with which venous hyperemia (stasis) is 
associated, the escape of the red corpuscles into the tissue, their 
disintegration, and the solution of the hemoglobin then occurs, and 
the solution enters the tubules, staining the dentin a pink color, 
which soon passes into a purplish rose, and finally becomes bluish- 
black or slate-gray. 

Those cases resulting in the yellowish or brownish coloration are 
usually associated with the loss of the pulp in comparatively sound 
or totally sound teeth, the loss occurring probably through trauma- 
tism or through slow atrophic changes, such as occur in the forma- 
tion of pulp nodules, secondary dentin, apical constriction, etc. 
Apical abscess is often much delayed, but sometimes occurs, showing 
that pulp decomposition or a later infection has occurred. The 
demonstration by Hopewell-Smith of fibrosis of the pulp and the 
obliteration of vascular structures may account for a lessened vas- 
cularity, and the absence of the production of iron sulphid because 
of the absence of necessary putrefaction and the production of the 
hematoidin products, as shown below. The first class of cases occurs 
either in sound teeth in which the pulps have died by traumatism, 
or in filled teeth with pulps not exposed, or in teeth the pulps of which 
are exposed to the fluids of the mouth, permitting putrefactive 
agencies and extraneous coloring or color-setting materials to enter. 
This discoloration is most rapid in the exposed cases. 

These color changes are rationally explained by Kirk 1 as due to 
the decomposition products of hemoglobin existing in the pulp at 

1 American Text-book of Operative Dentistry. 



506 GANGRENE OF THE PULP 

the time of its death, and having an analogue in the pigmentary 
degeneration occurring in the hemoglobin in a bruise (extravasation 
of blood), in which the part becomes, first, "black and blue," then 
passes through a series of color changes, in which yellow, green, and 
bluish-black are notable. These are due to new chemical compounds 
which crystallize in the tissue. These compounds are divided into 
two classes: Hemosiderins, or those containing iron, and hema- 
toidins, those without it. Each class of these has several distinct 
substances in it, each having its own color molecule. 

Kirk states that methemoglobin is brownish-red, hemin bluish- 
black, hematin dark brown or bluish-black, and hematoidin orange. 

Jakob (Stengel) gives light pea-green and brownish-red as the 
colors of hematoidin for an old hemorrhagic focus, showing a prob- 
able slight chemical variation in the composition of the color molecule. 

As the color changes in a bruise are effected under aseptic con- 
ditions, and usually the colors finally produced are lighter than 
the "black and blue" first resulting, it is rational to suppose that 
the yellowish or brownish discoloration of teeth results under such 
conditions of aseptic decomposition (probably autolysis). These 
colors, as remarked by Kirk, are more or less permanent. 

When a permanent or progressively darkening slate-gray or 
bluish-black color is produced, it is considered by Kirk to be due to 
the formation of iron sulphid or an analogous product in which iron 
and sulphur are constituents, and that it is analogous to the black 
discoloration occurring in the visceral walls of animals undergoing 
putrefactive decomposition. The iron is liberated from the hemo- 
globin present by putrefaction, and combines with the ammonium 
sulphid which is formed from the ammonium and hydrogen sulphid 
produced by the putrefactive decomposition. (Fig. 480.) 

Treatment. — The treatment of discolorations consists in what is 
known as the bleaching process, which means the reduction of the 
color molecule to another chemical molecule which is colorless, and 
then washing that out of the tubules. This is usually done by the 
use of chemicals which directly supply a molecule of nascent oxygen 
when coming in contact with the putrefactive material or its product, 
the color molecule; or which, as chlorin, abstract hydrogen from 
the water present and so liberate a molecule of nascent oxygen, 
which combines with the color molecule. These are direct or indirect 
oxidizing agents, the effect being the same, i. c, an oxidation of the 
color molecule. A second class, as sulphurous acid, which abstract 
oxygen from the color molecule, are called reducing agents, and may 
be effective when the oxidizing agents fail. 

In the use of bleaching agents the canal should have been cleansed 



MOIST GANGRENE OF THE PULP 507 

and disinfected with a simple aqueous solution of formalin or 25 per 
cent, ethereal pyrozone, or an aqueous solution of hydrogen dioxid, 
or with sodium dioxid, or kalium-natrium alloy, all oils or other 
materials likely to complicate the color molecule being avoided. With 
the exception of formalin, these are also bleaching agents and to an 
extent aid the subsequent operation. Formalin would best be avoided 
in cases of recent pulp death, as it may harden the undecomposed 
fibrils in the dentin. The upper half or two-thirds of the canal should 
then be filled with gutta-percha or oxychlorid of zinc, leaving the 
crown and one-third of the root dentin to be bleached. 

After accurate rubber damming the most valuable and facile 
method consists of wiping out with a strong alkali as sodium dioxid 
solution, etc., and placing a pellet of cotton saturated with 25 per 
cent, ethereal pyr ozone in the pulp chamber and sealing it after 
careful drying of the lingual tap or cavity orifice by dropping soft, 
quick-setting cement upon the margin and sealing the entire tap. 

The rubber dam should not be removed until the cement has set, 
as the ether or oxygen gas may cause it to bulge or blister. This is 
then allowed to have twenty-four or even more hours of action, when, 
if necessary, it may be removed. The operation may be watched at 
the first or the second sitting if desired, though it may be somewhat 
prolonged. 

Aqueous 25 per cent, pyrozone may be made by shaking together 
in a test-tube one volume of distilled water and two volumes of 
25 per cent, ethereal pyrozone and evaporating the ether, the H 2 2 
being left in aqueous solution; the addition of sodium acetate or 
sulphate assists the passage of the current. This is introduced by 
means of the cataphoric current, the positive pole being in the tooth, 
the negative at the hand. Occasionally the reversal of the pole 
succeeds after failure, the tubular contents probably being discharged 
with the H 2 2 present in them. 

Oxygen may be liberated from sodium dioxid (Na 2 2 ) by sulphuric 
acid. A saturated solution of sodium dioxid is made by surrounding 
a small beaker containing about 2 drams of distilled water, with 
cracked ice. When cold the sodium dioxid powder is to be slowly 
dusted into it until it assumes a semi-opaque appearance, indicating 
saturation. In use the dried dentin is saturated with it, asbestos 
fiber being used to carry it to place, and 10 per cent, sulphuric acid is 
used to produce the liberation of oxygen with the following equation : 
Na 2 2 + H 2 S0 4 = Na 2 S0 4 + H 2 2 . 

The effervescence forces the tubular contents out. The sodium 
dioxid acts upon putrefactive material, decomposing it, and also 
saponifies fatty matters. 



508 GANGRENE OF THE PULP 

If the operation fall short of success, this is due, in Kirk's opinion, 
to the formation of iron oxid, which can be removed with oxalic acid 
by sealing a crystal of it in the pulp chamber for twenty-four hours. 

The tubular contents being entirely removed by the sodium-dioxid 
method, the tooth is more translucent than by other bleaching 
methods in which the bleached organic debris remains in the tubules. 

The chlorin method, introduced by Truman, depends for its 
efficiency upon the affinity of chlorin for hydrogen, forming hydro- 
chloric acid (HC1). Finding this in the w T ater, it liberates nascent 0, 
which oxidizes the color molecule, or, possibly, it abstracts H from 
the organic matter. The chlorin is usually evolved from chlorinated 
lime, that sold in paraffined paper cartons or glass bottles being the 
best. That sold in metal cans is often contaminated by the metallic 
chlorids. 

The dry powder is packed into the cavity, moistened with 50 per 
cent, acetic acid, and sealed in with oxyphosphate or temporary 
stopping for one or two days, and repeated if necessary. Only vul- 
canite, bone, ivory, or wood instruments should be used, as metal 
instruments are acted upon by the chlorin. All gold or metallic 
fillings should be removed for the same reason, and if their removal 
would cause hardship or so render the tooth into a condition indi- 
cating crowning, either this should be done or the direct oxidizing 
method tried. 

The liberation of sulphurous acid may be induced from a powder 
consisting of a mixture of sodium sulphite, 100 grains, and boric 
acid, 70 grains, separately desiccated and afterward ground together 
in a mortar, by acting upon it with a drop of water. The cavity is 
stopped by a plug of gutta-percha previously prepared and warmed. 
The following reaction occurs: 

2H 3 B0 3 + 3Na 2 S0 3 = 2Na 3 B0 3 + 3H 2 + 3S0 2 . 

In all the methods, except the use of Na 2 2 , the apex of the canals 
should be sealed before bleaching; after bleaching at least 1 pint of hot 
distilled water should be forcibly injected into the tooth to dissolve 
out all products of chemical action remaining in the tubules, a towel 
being used to catch the drip. The tooth is then thoroughly dried, 
and if any organic matter may be present in the tubules the pulp 
cavity should be thinly lined with oxychlorid of zinc to coagulate 
it. If it has been removed, as in the sodium dioxid method, leaving 
the tubules empty, they should be filled with cavitin varnish after 
desiccation to promote absorption, and the thin lining then placed. 
A temporary filling is to be inserted over this until success is evident, 



MOIST GANGRENE OF THE PULP 509 

when the permanent work is completed with zinc phosphate and a 
metal filling. 

The removal of metallic stains has been referred to on page 238. 

Moist Gangrene of Pulps of Temporary Teeth. — The same con- 
siderations pertain to moist gangrene of the pulps of temporary 
teeth, but as the roots are resorbed to some extent or are to be 
resorbed, the root filling should be of such a character as to permit 
its resorption. Probably a combination of paraffin and aristol will 
best fulfil the indications. An iodoform paste is preferred by some. 
(See Root Canal Fillings.) 

If the roots be much resorbed, it is better to use a material which 
will permit venting of the tooth if necessary. The canals and pulp 
chamber may be filled with a combination of vaselin and aristol, and 
this covered by a filling. If trouble arise, a spear drill is driven into 
the pulp cavity from a point beneath the gum margin, establishing 
a vent. The patient should be instructed to keep this open, and be 
furnished a Swiss broach for the purpose. 

At an age when the permanent tooth will shortly thereafter erupt, 
extraction of the temporary tooth is often to be preferred to treat- 
ment. 

Root-canal Work in Cases of Gangrenous Pulps Involving Future 
Consideration. — In some cases of doubtful root sterilization or filling, 
and in which crowning by means of dowelled crowns is a necessity, 
provision may be made for future relief or treatment by the employ- 
ment of one of two excellent methods of procedure : 

1. Kirk has suggested that the post and band of a Richmond crown 
be painted while warm with a solution of gutta-percha in chloroform. 
The solvent evaporates, leaving a coating of gutta-percha. This 
should be reasonably thick. The crown is then tried in the wet root 
and later all being dried it is set with cement. By warming the crown 
with a hot crown-setting tool (How) or copper ball or perhaps forceps, 
it may be removed without destruction of the piece. Bridges so set 
are very firm. To insure removal of shell crowns their undercut 
should be filled with gutta-percha and the piece set after trial. The 
crown may be set with gutta-percha alone or in some cases with 
temporary stopping. 

2. Gird wood (Edinburgh) has suggested root intubation, the tube 
being closed at the end with temporary stopping and then set with 
cement. Immediately thereafter the temporary stopping and soft 
cement are removed with Donaldson cleansers, leaving the root 
lumen free to the apical foramen or root filling. The tube and canal 
are then treated as a continuous root canal would be. The idea is 
also applied to a Richmond or all-porcelain crown, the tube being 



510 GANGRENE OF THE PULP 

used in place of the pin, and allowed to extend through the backing, 
to be later filled as desired. 

In certain cases, as after removal of artificial crowns for root treat- 
ment, or during construction of new ones, a temporary crown is needed 

1. A cross-pin facing is adjusted to the labial cervix only; a soft 
German silver wire is adjusted to the canal, notched at the line of 
the pins; the pins bent around in the notch, asbestos paper wrapped 
and wired around the labial of the facing, soft -solder and zinc chlorid 
solution placed at the pins and heat gently applied to the asbestos 
over a Bunsen burner. A slight adjustment of the not too stiff pin 
may be necessary. It is set with temporary stopping or preferably 
base plate gutta-percha, allowing it to make the adaptation and hold 
back the gum. Iodin is first applied for sterilization. Tagger sug- 
gested a copper pin to be beaten flat at one end and this portion 
appropriately punched. The pins are inserted and soldered as 
above or bent down. 

2. Use a Goslee facing, adjust crown and pin, try in together while 
loose; dry both; cement pin in crown; apply to root while soft for 
adjustment, remove, await hardening, set with gutta-percha as before. 
In either case when the crown is recovered, clean and sterilize it for 
future use. 



SECTION VII. 

DISEASES OF THE PERICEMENTUM. 

CHAPTER XVI. 
PERICEMENTITIS. 

Classification — The pericementum, is the seat of numerous nutri- 
tive and functional disturbances, which may be grouped, according 
to their causes, into septic and non-septic. 

The term pericementitis has been indiscriminately applied to all 
affections of the pericementum, and in some cases erroneously, for in 
not all affections of this structure do the phenomena of inflammation 
appear; in some hyperemia alone may exist. (See Hyperemia of 
Pulp.) However, most of the acute and chronic degenerations are 
accompanied by evidences of inflammation. 

The most convenient clinical classification of these disorders is 
that offered by G. V. Black: 1 (1) Diseases of the pericementum 
beginning at the apex of the root; (2) those beginning at the gum 
margin; (3) those beginning in some intermediate portion of the 
pericementum. These may again be divided, according to their 
causes, into septic and non-septic. Another clinical classification 
would be into localized and general disturbances — another into acute 
and chronic. 

Evidences of Pericemental Disturbance. — Disturbances of the 
pericementum are accompanied by entirely different symptoms 
which serve to distinguish between them and diseases of the 
pulp. They are, in general, tenderness upon percussion. As 
shown by Black, 2 the pericementum is the touch organ of the tooth, 
its tactile organ, through which a tooth locates force applied to the 
tooth. The pains of pericemental disturbance are, therefore, in the 

1 American System of Dentistry, vol, i, 2 Ibid. 

(511) 



512 PERICEMENTITIS 

majority of cases, exactly localized, instead of not being localized, 
as in the case of the pulp. A tooth tender upon percussion has 
its pericementum as the seat of disturbance, at least there is a peri- 
cemental disturbance there primarily such or as a result of pulp 
disturbance. Most cases of pericemental diseases are accompanied 
by vascular reactions ranging from an increased blood flow, or grades 
of hyperemia to pronounced inflammation, and have the corre- 
sponding symptoms. The increased volume .of the pericementum 
causes the protrusion and loosening of the tooth, heightened sen- 
sitivity being the accompaniment. As the vascular supply of the 
pericementum and that of the gum are in a degree collateral in 
advanced cases, evidences of vascular engorgement may be seen in 
the gum overlying the affected tooth. Owing to the altered density 
of the parts surrounding the tooth root, percussion upon the tooth 
elicits a different sound from that observed in health — the sound is 
dull. The general symptoms of pericemental affections are, therefore, 
tenderness upon percussion and a dull percussion note, more or less 
protrusion, and looseness of the tooth and a deepening of the local 
gum color, but in cases of granuloma and blind chronic apical 
abscess there may be no subjective or local symptoms of disturb- 
ance cognizable to patient or operator. Hopewell Smith 1 has 
claimed that there is no appreciable movement of normal teeth "in 
their articulations." There is against this the clinical fact of move- 
ment with steel wedges, by inflammation, etc., which are merely 
exaggerations of the normal and the dull note obtained by striking 
a normal tooth as compared with the sharp note obtained from an 
implanted tooth in which bony fixation occurs with perhaps penetra- 
tion of slightly resorbed cementum by newly formed bone. 



DISEASE OF THE PERICEMENTUM BEGINNING AT THE APEX. 

Diseases of the pericementum beginning at the apex of the root 
are of two classes, septic and non-septic. The septic cases are almost 
invariably the sequel to necrosis of the pulp, at least in one root of a 
multirooted tooth, by suppuration or gangrene, the canal being septic 
or arise in consequence of infection through the canals of pulpless 
teeth. The non-septic cases are due to mechanical and chemical 
irritation, and in rare cases to undiscovered causes. 

Septic Apical Pericementitis; Apical Abscess. — Definition. — By 
septic apical pericementitis is meant an inflammation of the apical 

1 Dental Cosmos, May, 1918, page 426. 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 513 

pericementum due to the entrance of bacteria into the tissue lying 
in the apical space. 

The apical tissue may actively resist a comparatively mild or so- 
called non-virulent infection, such as due to Streptococcus viridans 

Fig. 490 




Alveolar abscess pointing externally. The abscess is caused by the only-slightly- 
impacted and not-malposed lower, third molar. (Raper). 



and may proliferate by cell multiplication into a more or less solid 
mass of soft tissue known as a granuloma or the tissue may be rapidly 
broken down into pus through suppurative inflammation due to more 
virulent infection, a condition known as acute apical abscess. The 
33 



5 1 4 PERICEMEN TI TIS 

granuloma may develop an acute phase later or may contain a small 
chronic abscess within itself. It will be considered later on. 
Naturally there may be gradations in these two classes of reactions. 

Causes. — The most common causes of acute septic apical peri- 
cementitis and chronic septic apical pericementitis are: 

1. Bacteria engaged in the putrefaction of a gangrenous pulp. 
The gases and toxic products evolved by the process also cause 
much irritation. 

2. Pyogenic organisms engaged in the production of suppuration 
of the pulp in its later stages. 

3. Pyogenic organisms introduced into the otherwise aseptic tissues 
of the apical space by means of instrumentation or other lack of 
aseptic precautions, or if asepsis has been observed in root filling a 
later sepsis may occur via spaces about the root filling. 

4. An acute outbreak from a true blind abscess or granuloma which 
will be later described under the heading of chronic abscess, (page 555.) 

5. Infection of an apical space by an abscess arising in some con- 
tiguous part and extending in the direction of the apical space under 
consideration. Even antral empyema caused by sinusitis may do this. 

6. Septic infection from a pyorrhea pocket located upon the side 
of the tooth in question, the deepest portion of which approximates 
the apical space. This may act in two ways: (1) by direct infection 
of apical tissue from the pocket; (2) by pulp infection abscess subse- 
quently appearing (a Class I case). 

7. Possible infection by way of the pericemental tract from the 
gum margin which infection may cause a pericemental abscess 
located in the apical tissue. The pericemental abscess in this location 
seems rare and differs as a cause of apical abscess from Class VI cases 
only in having an apparently unbroken gum margin. If such an 
opening exist, no matter how puzzling it is a Class VI case. 

8. Occasionally a suppuration following a severe fracture of the 
alveolar process might include the apical tissue as sometimes acute 
apical abscess follows such a fracture. 

9. Infection by way of the circulation, as for example, in influenza 
or tonsillitis, in which the bacteria are in the blood or from some 
other focal infection (see page 557). The theory is that said bacteria 
locate in the apical tissue of perhaps properly treated roots and cause 
effects. It is noted that at times when colds or tonsillitis are general. 
usually in changeable weather and temperatures, abscesses appear 
more frequently. A. D. Black 1 comments that this is due to infective 
attack via the circulation upon quiescent granulomata. 

1 Journal of Allied Societies, 1917. 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 515 

Apart from these causes infective inflammation of apical tissue 
does not seem to occur. It is to be remembered* that a small portion 
of gangrenous pulp beneath a root-canal filling is equivalent to an 
entire gangrenous pulp as a cause of pericementitis. The vast 
majority of cases occur as a sequel to putrefaction of the pulp, 
either before or after instrumentation, or as a result of infection of 
the apical tissue by instruments either unsterilized or reinfected by 
contact with the oral fluids, septic fingers, etc. 

The organisms found in acute apical abscesses are those usually 
found in gangrenous and suppurating pulps, and in a certain per- 
centage of even healthy mouths. Schreier found the Diplococcus 
pneumoniae in 15 out of 20 cases examined. He also found Staphy- 
lococcus pyogenes albus and aureus, and occasionally Streptococcus 
pyogenes. Streptococcus viridans is also found. 

Arkovy found the Bacillus gangrenae pulpae in a number of 
cases. These are virtually the same organisms that are found in the 
deeper portions of a suppurating or gangrenous pulp; this fact 
in itself is enough to show the continuity of infection from the 
pulp canal. 

The large number of blind abscesses and granulomata found on 
painless devitalized teeth by radiography as compared with but 
occasional cases of acute abscess seems to show that many of the 
latter are Class IV cases and that the infections are resisted by the 
tissues until some increased virulence or lessened resistance, or perhaps 
added infection (Class III or Class IX) occurs. Clinically in a number 
of cases a hard bite producing pains had started acute symptoms 
presumably through compression of a granuloma with disturbance 
of its balance of resistance to infection. It is sometimes difficult 
to distinguish between a non-septic apical pericementitis and a septic 
apical pericementitis if no pus is present; if, however, pus is produced 
resulting in an acute suppurative process the condition of acute 
apical abscess is produced to which the following description refers. 

Pathology, Morbid Anatomy, and Symptoms. — The Inflammatory 
Stage. — As in abscess elsewhere there is first infection by pyogenic 
organisms which produce the phenomena of infective inflammation 
within the substance of the apical tissue, and in the later stages in 
the contiguous tissues. (See page 41.) 

Following the infection, arterial hyperemia is produced, sensation 
is exalted, and the tooth becomes tender upon percussion; but if 
forcibly pressed upon — i. e. } if the arteries be compressed — the 
hyperemia is momentarily lessened and the pressure brings a sense 
of relief. At this stage the gum over the apex looks normal, but 
may respond to pressure, 



516 



PERICEMENTITIS 



Following the arterial hyperemia, the venous obstruction which 
ends in stasis is inaugurated and diapedesis of leukocytes and fibrin- 
ous exudation into the intervascular tissue occurs. The fixed cells 
undergo proliferation. (See page 36.) 

As this condition of inflammation becomes established the pain due 
to pressure upon the sensory nerves becomes of a violent throbbing 
character, accompanied by a sense of fulness. The swelling of the 
tissue about the apex of the root, due to the excess of fluid, blood, 
leukocytes, and tissue cells, of necessity pushes the tooth from its 

Fig. 491 




Stowing the morbid anatomy of septic apical pericementitis (acute): A, pus; B, 
area of dying leukocytes; C, septic matter in root canal; D, inflammation of process 
(osteomyelitis; area of lesser inflammation); E, swollen periosteum and gum, hyper- 
emic; F, alveolar bone in a stage of hyperemia; G, pericementum at edge of necrosis. 



socket, so that it feels and is longer than the other teeth. Moreover, 
as it is bitten upon the apical tissue is further irritated. The tooth is 
loosened and percussion induces pain and elicits the dull note which 
is diagnostic of the increase of bulk in the pericementum. The color 
of the gum over the root becomes deepened. 

First Stage of Pus Formation. — The central area of the apical 
tissue — -i. e., that next the apical foramen or small areas nearby — is 
broken down into pus, some of which enters the root canal (Fig. 491, 
A). As the area of pus formation widens much of the apical tissue is 
liquefied (Fig. 493, a), though the fibers are quite persistent. From 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 517 

a clinical point of view the abscess is incipient when inflammation 
of the apical tissue next to the foramen is profound, and pus formation 
has just begun (Fig. 491). The first stage continues while the pus is 
in the apical tissue. 

The surrounding tissues are necessarily inflamed, reddened and 
swollen in proportion to the extent of pus formation. Even when the 
pus is still in the apical space the gum and immediately surrounding 
lip or cheek tissue may be inflamed, but often no such direct evidence 
may be obtained even when pus is evacuated via the canal. 



Fig. 492 



Fig. 493 





Abscess on crowned root. (Radiograph Acute abscess in second stage. Tooth 

by Lodge.) opened at b. for treatment, making an 

abscess, discharging via the canal. (Black.) 



Fig. 494 



Fig. 495 




A cyst extending from left lower second bicuspid to 
the central of same side. The central has a root filling. 
In absence of other things this may be regarded as the 
origin of the cyst. 







Method of accurately de- 
termining length of root. 



Second Stage of Pus Formation. — The bone cells become 
involved in the process and are destroyed (osteitis). The throbbing 
pain, the extrusion, looseness, and dulness to percussion, and the 
inflammation and edema of the contiguous tissues are marked. The 



51S 



PERICEMENTITIS 



Fig. 496 



gum is widely inflamed, reddened, and swollen, but no demarcation 
of an abscess may be noted upon the gum at this stage. The mem- 
branes of the adjoining teeth become irritated and hyperemic, and 
they may exhibit tenderness upon percussion and their pulps may 
show evidence of arterial hyperemia. There may be a fair involve- 
ment of surrounding tissues. 

Third Stage of Pus Formation. — The pus continues to form 
in all directions until the bone is perforated at some point — i. e., 
usually through the labial alveolar plate — that being the thin- 
nest and most readily per- 
forated. The periosteum is 
now raised and with the gum 
tissue directly involved as a 
boundary to the pus, which 
collecting beneath it, raises it 
into a distinctly demarked 
tumefaction (Fig. 496, 6). The 
pain becomes less acute, owing 
to the binding resistance of 
the gum being less than that 
of the bone. At first the 
swelling is hard, and this 
represents a mass of gum tis- 
sue overlying pus; later, it 
softens at its highest point, 
pus appears as a yellow spot 
beneath the mucous mem- 
brane. The mucous mem- 
brane bursts and a discharge 
of pus follows. The inflam- 
mation and tenderness then 
largely subside, but some de- 
gree of looseness and protru- 




Acute alveolar abscess of a lower incisor in 
the third stage, with pus cavity between the 
bone and the periosteum: a, pus cavity in 
the bone; b, pus between the periosteum and 
bone; c, lip; d, tooth; e, tongue. (Black.) 



sion remains. 



During the latter part of the second and in the third stage of pus 
formation, instead of the swelling extending but little beyond the 
overlying gum, the tissues of the lips, cheeks, or neck may be very 
much swollen and with upper teeth the eye of the affected side 
injected. In some cases the outer skin may become reddened and 
dusky, exhibiting the evidences of extension of the inflammatory 
process far from its original site. 

The inflammatory process spreads out from the central focus of 
pus formation, there being around the pus a zone of active inflamma- 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 519 

tion or stasis; about this one of a lesser degree of inflammation, also 
full of leukocytes; about this an area of arterial hyperemia or the 
first stage of inflammation, and around this normal tissue. These 
areas are not sharply defined, but merge into one another (Fig. 491, 
B, D, E, F). 

In this way the contiguous area of the alveolar bone and the soft 
tissues of the face become involved in the process, being discolored 
and tumefied in proportion to the extent of the pus formation and 
the inflammatory reaction thereto, the facial swelling is largely due 
to inflammatory exudate into subcutaneous cellular tissue spaces 
and a better idea of the possibility can be obtained by a considera- 
tion of the facial emphysema described on page 504. This swelling 
may be very great even with a moderate amount of pus. 

While in the vast majority of cases the direction taken by the pus, 
and the point at which it finds exit, is the buccal or labial aspect, and 
immediately over the root apex of the affected tooth, or near it, 
these being the directions of least resistance, other anatomical con- 
ditions or histological peculiarities may make the direction of least 
resistance in some other path (Figs. 497 to 501). 

Instead of the circumscribed suppuration described as the ordinary 
course of abscess formation about the apices of roots (septic apical 
pericementitis) which accompanies infection by the staphylococci, 
clinical evidences of infection by streptococci occasionally appear. 
The inflammatory process, instead of being circumscribed, is diffuse; 
the inflammation extends along the lines of the connective tissues 
and of the lymphatics; the connective tissues are swollen, the swelling 
extending to the tissues of the cheek, down the neck, and even to 
the shoulder — a phlegmonous inflammation. Instead of the com- 
paratively free flow of pus which follows incision of the swelling in 
ordinary abscess, pus formation in streptococcus infection is seen, 
upon incision, to be limited and seropurulent. While in alveolar 
abscess of the ordinary types evidences of septic intoxication or 
poisoning are unusual, the lymphatics being blocked, as a rule, by 
the inflammatory exudates, septic intoxication and poisoning are the 
rule in the erysipelatous cases, those probably due to streptococcus 
infection; bacterial poisons being taken up by the lymphatics find 
their way into the circulation. 

The symptoms of the absorption of bacterial products from the 
circumscribed abscesses are: Fever, often ushered in by a distinct 
chill. The pulse increases in volume and tension; it is full, hard, 
and frequent. The tongue is coated, the bowels constipated. The 
patient is also weakened and made irritable by pain and attendant 
loss of sleep and appetite. 



520 PERICEMENTITIS 

In the streptococcal infection there is danger that these may 
change into the more profound symptoms of septicemia — L e., a 
soft, frequent pulse, repeated chills, diarrhea, clammy skin, general 
depression, and a disordered nervous system. 

In multirooted teeth the inflammation and abscess frequently 
appear on only one root. If the case be seen early, before the active 
exudation period of the inflammation sets in, the symptoms may be 
clearly localized in one root, the tooth exhibiting tenderness upon 
pressure over the affected root, but not upon the opposite side; in other 
cases more than one root are involved. Radiography is a more certain 
guide but is confused in some cases especially upper molars. 

After spontaneous discharge of the pus from an abscess, the 
condition remaining is that of an ulcerous surface (the abscess 
boundaries) which is being continuously infected from the putrescent 
pulp remnants. The conditions, it is seen, are not like those of 
ordinary abscess, where the infective material is largely discharged 
in the pus evacuation, and the cells bounding the abscess wall 
dispose of remaining bacteria, so that regeneration of tissue occurs. 
Spontaneous healing of an apical abscess is the exception; the 
embryonic tissue lining the abscess walls, being continuously infected, 
degenerates and dies as fast as it forms, leaving a condition known 
as chronic apical abscess, which will later be described under that 
heading. 

Clinical History. — The clinical history of acute alveolar abscess 
may be divided into three stages: (1) That of initial inflammation 
and pus formation; (2) the destruction of the alveolar process; (3) 
the passage of pus through the periosteum and mucous membrane. 
The second stage is usually the longest. The duration of the disease 
depends upon the readiness with which the tissues between the point 
of beginning pus formation and its exit yield. When the pulp 
chamber is open pus may find exit by this path, constituting the 
condition formerly known as blind abscess — a misnomer, because a 
blind abscess is one without a point of discharge, without a fistula 
leading to it; in the cases discharging via the canal, the latter may 
be considered a fistula (Fig. 493). 

Acute abscesses usually run a short course, the inflammatory 
symptoms being severe and the tissue destruction limited. Notably 
upon lower molars, and upon the lingual roots of upper molars, 
the density and thickness of bone overlying the roots may make 
paths of greatly increased resistance, so that the destruction of 
tissue proceeds along the line of the pericementum, the pus finding 
exit at the neck of the tooth. It is rare in cases of lower second 
molars, and still more rare upon the third molars, that pus finds 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 521 

exit over the apex of the root, the dense bone of the external oblique 
line offering the greatest resistance (Fig. 497). Over any teeth 
the outer fibrous layers of the external periosteum may present 
unusual resistance to the perforative advance of pus, so that when 
the fibers of attachment of the periosteum have been softened by 



Fig. 497 



Fig. 498 





Abscess upon lower third molar, 
showing the usual paths of pus exit, A 
and B. 



Abscess upon palatal root of an upper molar 
discharging at the neck of the tooth. 



Fig. 499 



the inflammation, and pus gains entrance between bone and peri- 
osteum, it may travel or burrow along the course of this membrane 
(Fig. 498), depriving the bone of its main nutritive source, so that 
limited necrosis threatens. The roots of the central incisors may lie 
unusually close to the floor of the nose, 
and be overlaid externally by an unu- 
sually resistant layer of bone; in these 
cases the path of least resistance may 
be in the direction of the floor of the 
nose, the abscess opening at that point 
(Fig. 500), or the pus may perforate 
the lingual alveolar plate, and, raising 
the periosteum and mucous membrane, 
form a large swelling upon one side of 
the hard palate. 

Vederspiel 1 instances a case in which 
an abscess starting upon an upper third 

molar finally infected the tonsil producing an abscess, also produced 
necrosis of a portion of the ramus of the inferior maxilla. 

The root apices of the posterior upper teeth, particularly of the 




Lower molar with abscess and 
distal root persistently discharg- 
ing at gingival margin. 



1 Dental Cosmos, December, 1912. 



522 



PERICEMENTITIS 



first and second molars, may, after the age of twenty-five or thirty 
be encroached upon by the enlarging maxillary sinus, or may naturally 
lie in this position as in a skull of a woman of twenty-two years in the 
writer's possession, so that any or all of the roots of these teeth may 
be separated from the floor of the sinus by but a very thin lamina 
of bone or only by periosteum and mucosa; should abscess arise, 
upon any of these roots, pus discharge into the antrum would neces- 
sarily follow. In these cases the acute symptoms may rapidly subside, 
but later symptoms of antral empyema may follow (Fig. 501). 

Resort to the use of poultices upon the face, for the relief of the 
pain of abscess formation, may induce such a softening of the tissue 
over which they are applied that the passage of pus is invited toward 
the exterior; the abscess may thus open upon the face or neck, 
producing permanent, disfiguring scars (Figs. 490 and 533). 




Alveolar abscess at the root of a 
superior incisor, discharging into 
the nose: a, large abscess cavity in 
the bone; b, mouth of fistula on 
the floor of nostril; c, lip; d. tooth. 
(Black.) 




Alveolar abscess at the root of an upper 
molar discharging into the antrum of High- 
more: a, abscess cavity in the bone; b, 
mouth of fistula on the floor of the antrum; 
c, pus in the antral cavity. (Black.) 



In patients who are in a cachectic condition, who have an evil 
heredity, or whose tissue resistance is markedly lessened in conse- 
quence of tuberculosis, or more frequently of syphilis, septic peri- 
cementitis may run a riotous course; the bone suffers extensively by 
direct action; the periosteum is undermined, is stripped from the 
bone over large areas, and breaks down readily; so that while in 
the healthy person alveolar abscess formation may run a direct 
course and find prompt outlet, in the debilitated patient extensive 
pus infiltration, with necrosis, may occur. Thus an abscess on a right 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 523 

lower molar has been seen to dissect its way around the entire labial 
surface of the mandible to the left side. In cachectic persons lym- 
phatic involvement is common; waste products of bacterial origin 
find their way into the lymphatics, and set up secondary irritative 
processes in the nearest lymphatic glands — lymphadenitis. Acute 
systemic toxic effects are also produced. 

In persons whose oral hygiene is neglected the third stage of 
alveolar abscess is frequently violent and the inflammatory process 
widespread. 

Diagnosis. — In incipient apical pericementitis the symptoms may 
consist of reflex pains, but, as a rule, are distinctly localized in the 
teeth affected, which are tender to the touch. The discoloration of 
the tooth crown and other evidences of moist gangrene are usually 
present unless the tooth has been previously partially treated, when 
the color may be good, but by transmitted light opacity is noted. 
In a few cases the tooth has had almost a normal color even under 
the transmitted light. As color is not always a guide, electric, thermal 
or other tests for pulp vitality are in order in doubtful cases (see 
page 483). In the pronounced cases the symptoms are as described 
(see page 516, etc.). 

A timid patient will often unintentionally confuse pericemental 
tenderness with the pain of sensitive dentin. 

In very doubtful cases, as when molars have deep amalgam fillings, 
or pins have been placed in root canals, or gold crowns cover the 
natural crowns, either the covering 
must be removed or preferably a radio- FlG - 502 

graph be taken. 

After high inflammation has existed 
for twenty-four hours, pus is generally 
present in the apical tissue. 

Of two pulpless teeth surrounded 
by a zone of inflammation, the more 
tender and loosened is the one affected, 
though both may be acting at once. 
It is to be remembered that adjoin- 
ing, otherwise normal, teeth may show T 

. , p . , . , . , Diagnosis of apical abscess by 

some evidence ol pericementitis, due x-rays. (Price. 1 ) 

to extension, so that differentiation 

is necessary. Fig. 543 shows a lateral apparently affected. It w r as 

drilled only to find the pulp alive. This shows the need of confirm a- 

1 Items of Interest, 1901. 




524 



PERICEMENTITIS 



Fig. 503 



tory tests (see page 483). The various stages of inflammation and 
pus formation are judged by the appearance of the gum or by the 
.r-rays (Fig. 502). The greater the swelling and injection of the 
gum, the more advanced is the pus formation. 

The inflammatory action precedes the advance of pus, which 
furnishes a guide to the direction the pus is pursuing — viz., where 
the most intense coloration and the greatest swelling appears will be 
the point at which the abscess will point or .discharge. A sudden 
subsidence of inflammation without an immediately discoverable 
point of pus exit should lead to the suspicion that the discharge has 
taken place in an unusual situation. 

The direction pus may take is often determined by gravity, but 
the resistance of certain tissues may cause the pus to seek the easiest 
path. Thus, by discharging into the antrum or nose it goes counter 
to gravity. In such cases as discharge into the antrum there is 
liable to be a collection of pus in that cavity which may cause destruc- 
tion of the mucous membrane and bone. This condition is known 

as empyema of the antrum. The 
sudden subsidence of an acute abscess 
upon a tooth located beneath the 
antrum should create a suspicion of 
discharge into that sinus. If a fine 
probe can be passed an unusual length 
into a root canal it indicates this form 
of sinus involvement. 

An abscess originating about an im- 
pacted tooth, or one due to subperio- 
steal inflammation, must be differen- 
tiated 1 (Fig. 503). A pericemental 
abscess must also be considered. It is 
always more lateral and there is less 
facial involvement, also there is usually 
a pyorrhea pocket leading to it. An 
acute abscess of the pulp in its most 
pronounced stage may simulate incip- 
ient or even pronounced acute apical pericementitis. (See page 412.) 
An abscess sometimes forms beneath the flap of gam overlying a 
third molar. This begins as an ulceration of the under side of the 
flap, but the pus burrows between the tooth and the gum, and when 
well confined may develop laterally, causing the formation and at 
least partial retention of a quantity of pus in the tissues of the cheek. 




Non-descended cuspid and lat- 
eral. These teeth were entirely 
enveloped in pus. The cuspid 
and lateral shadows overlie each 
other. Between these and the 
first bicuspid may be seen three 
tiny supernumeraries. (Lodge.) 



Black: American System of Dentistry, vol. i. 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 525 

This condition more nearly simulates the lateral abscess associated 
with a pyorrhea pocket, and as by extension it sometimes involves 
the tonsil, the case may be mistaken for an amygdalitis. 

The last three conditions are usually associated with suspected 
teeth containing vital pulps, so that tests for pulp vitality are to be 
applied. 

In certain cases of pulp gangrene part of the pulp only may be 
dead — e. g., the lingual filament of the pulp of an upper molar; while 
the balance may be vital (the buccal filaments). This fact may con- 
fuse the response to tests and is to be borne in mind (see page 383). 
A broken root covered more or less by gum or carious bone must be 
taken into account (Fig. 307) . An ulcerated aveolar socket is usually 
obvious. 

Prognosis. —The writer believes that if proper root canal work can 
be done the parts can be sterilized and the roots aseptically filled so 
as to cure an acute apical abscess. This conclusion is, however, subject 
to the considerations on pages 467 and 469. The future of the tooth 
depends upon the thoroughness with which sources of infection may 
be destroyed and permanently removed, and the completeness with 
wilich regeneration of tissue can be induced. 

Treatment. — In the initial inflammation and first stage of pus for- 
mation the treatment should be abortive, to afford relief from the 
pain. The cause of the inflammation should be removed, if possible, 
and the pus formed be removed or, at least, permitted to escape by 
way of the pulp canals. The promptness of relief from pain depends 
upon the thoroughness with which this is accomplished. 

The pulp chamber should be opened to an extent which permits 
the free passage of broaches into the canal (Figs. 493 and 498). 

If the cavity of decay be open, the pulpal wall is to be perforated. 
If a filling be present, it is in part or entirely removed. If the enamel 
be entirely sound, or if subsequent treatment require a new opening 
in line with the pulp canals, it is at least in part made. 

These openings are usually begun with a small, spear-pointed drill 
(No. 100, S. S. W. Catalog) revolving in a perfectly true hand piece. 
To center the drill, first spot the enamel with a dentate bur. The 
opening made is enlarged with successive sizes of sharp, round, 
dentate burs until of sufficient size. 

According to the amount of tenderness, the tooth will require a 
counterpressure to that of the drill. If the entrance be made through 
the occlusal face of the tooth, or in a direction which would cause 
direct pressure on the apical pericementum, a ligature of the traction 
cable now used -forwedging with long ends may be placed around the 
tooth, and traction be/nade by drawing on the loose ends of the liga- 



520 PERICEMENTITIS 

ture. 1 Effective coimterpressure against lateral entrance to the pulp 
chamber may be made by softening a small roll of modeling compound 
and moulding over the face of the affected tooth and several of those 
adjoining it, and hardening with cold water. This temporary splint 
is held in place by the index finger of the left hand. W. D. Tracy 
recommends for posterior teeth a double modeling compound splint, 
one lingual, one buccal, to be held with the fingers, or two ligatures 
may be placed between the teeth before the compound is placed and 
the ends tied over the splints, binding them against the teeth. A special 
clamp raising the affected tooth can be had of J. W. Ivory. In case 
the inflammatory process is marked, or if the patient be in bed, it 
may be necessary to make a vent opening by the easiest path, espe- 
cially when using a hand drill — i. e., at the junction of enamel and 
cementum — directly into the chamber. 

Watkins 2 has used "blue light" applied from a 16-candle power 
blue-globed electric lamp through a funnel directly upon the part. 
He claims relief from the pain, enabling him to open the tooth 
previously too painful to be operated upon. He also claims that 
swelling is much reduced by it, in some cases in twenty minutes. 
The high frequency current is also useful in this connection. The 
broad electrode of a violet-ray apparatus is applied to the face and 
moved about. (See Chapter on Uses of Electricity.) 

Patients do not ordinarily tolerate the rubber dam in these cases, 
and as the tooth should be left open it need not be used. 

As soon as entrance to the pulp chamber is effected, the cavity 
is syringed with a strong antiseptic. Fine probes are passed and 
repassed into the opening to free the outlet, so that gases and pus 
may escape and fresh portions of the antiseptic be worked into the 
cavity. The escape of blood from the canal is a sign that all the pus 
is vented. The quickness with which relief is secured will depend 
upon the thoroughness with which the canals are entered and their 
putrid contents given vent. A tedious class of cases are those in 
which a canal of a molar is filled or partially filled. Unless entrance 
to and cleansing of the canal be accomplished, the inflammation 
will proceed until the pus finds external vent. An hour spent in 
gaining access to and cleansing such canals is well spent. 

The patient may be directed to make suction with the tongue 
to create a vacuum tending to draw the pus, etc., into the canal. 
If a tight joint can be obtained with a special point an abscess syringe 
may have its plunger drawn back to create the vacuum. This 
measure is not necessary when prompt relief is obtained by venting. 

1 J. Foster Flagg: Lectures on Dental Therapeutics. 2 Dental Cosmos, 1905. 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 527 

The canals may be dried and an anodyne antiseptic, such as 
phenol camphor plus menthol, pumped into them. If, now, pro- 
vision against mastication upon the elongated tooth be made by 
means of a guard, relief is tolerably certain. 

A guard may be made from a strip of rubber dam two inches long 
and of a width corresponding to the distance from the buccal to the 
lingual gum margins and rolled into a pad of the width of the 
occlusal face of the tooth to be covered. Floss silk is then sewed 
through this in such a manner as to cause it to tie the pad over the 
tooth, the silk itself encircling the neck of the tooth. 1 This should 
be attached to a nearby tooth, and will insure rest of the affected 
pericementum by preventing occlusion upon the abscessed tooth 
(Fig. 504). 

Fig. 504 





Rubber dam guard for use in pericementitis: A, roll of dam threaded; B, guard fitted 
over tooth; tooth eliminated to show the manner in which the silk encircles it. 



The mouth is to be frequently washed with a cold antiseptic (Lis- 
terine in hamamelis). In simple cases with prompt relief this is 
all that is necessary; in marked cases the reduction of the inflam- 
matory engorgement should be attempted in addition. 

1. In some cases application of cold wet cloths or an ice-bag to the 
face is a sufficient addition. In more marked cases, one of several 
lines of treatment may be added. Swedish leeches may be applied 
to the gum, or a cut or two made in the gum over the apex of the 
tooth will allow free bloodletting and drainage of the excess of blood 
in the pericementum. A tablespoonful of magnesium sulphate in a 
goblet of water or a bottle (12fg ) of citrate of magnesia is given as a 
derivant and depletive. Also a hot pediluvium with mustard added 
is administered as a derivant. Quinin in doses of gr. vj is given as 
a febrifuge and to limit exudation, and tincture of aconite, two drops 
at first, and one-half drop each half hour is given until the volume, 
tension, and frequency of the pulse are reduced. 

Morphin sulphate in blondes and morphin bimeconate in brunettes, 
especially those with blue eyes (or any persons with known idio- 

1 Flagg. 



528 PERICEMENTITIS 

syncrasies to morphin), may be administered in f -grain doses, repeated 
each hour up to f grain. When great suffering renders it necessary, a 
hypodermic may take its place. Trigemin, bromural and aspirin are 
alternate anodynes after the bloodletting, etc. 

2. The hot pediluvium is to be administered and during this a 
portion of a solution of 10 grains of Dover's powder in a quantity 
of hot lemonade is drunk. Later when the patient is well covered 
in bed the balance is taken. This treatment conjoins — derivation by 
pediluvium and diaphoresis and an anodyne'. 

As the opium taken equals f grain of morphin, if needed more mor- 
phin may be used. 

Quinin gr. vj and the aconite as before may be used. 

These several measures are to be regarded as the abortive treat- 
ment of alveolar abscess ; they apply to all cases if seen early enough, 
and will in the majority of cases prevent the disease passing the 
early inflammatory stages, unless septic matter be violently thrust 
through the apical foramen, especially of the one of a multirooted 
tooth which is not involved. 

The Second Stage of Acute Apical Abscess. — The pus is in the bone 
and the infection considered more virulent, i. e., the germs are 
especially active. The abortive treatment should first be tried, and if 
free venting of pus is obtained relief is usually given. If not given the 
case continues to the third stage. If bearable, or the surgical method 
be impracticable, a dental capsicum plaster may be applied to the 
gum or a roasted half -raisin may be applied. Either causes an inflam- 
mation of the gum, which advances the tissue that much nearer 
suppuration. Thus it prepares a readily invaded tissue and hastens 
pointing. The contrary effect has sometimes been produced, and is 
explained upon the ground that the increased amount of blood 
has increased the phagocytosis and destruction of bacteria or has 
stimulated a restoration of the circulation, possibly both, producing 
resolution. It is proper to denominate this the expectant treatment, 
and while, perhaps, unsurgical, at times permits no alternative 
except extraction. The pain is to be combated with anodynes. 

When tolerable or imperative, the surgical method of venting the 
abscess through an opening in the gum is valuable. The apical 
region is located as nearly as possible by measuring the length of the 
tooth with a probe passed into the canal and over which a small 
piece of rubber dam is slipped as a guide. This is laid over the 
crown and gum and a tiny drop of carbolic acid is placed just above 
the point of the probe as a guide. A vertical cut is made in the 
gum down to the bone, and a broad spear drill is driven through it 
into the abscess tract. Whether this shall be done under ethyl 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 529 

chlorid refrigeration, local or conductive anesthesia, or short general 
anesthesia, the operator must determine. 

A gradual perforation is useful in some cases. This method, 
designed by Black, consists in gradually escharing and scratching 
the gum tissue. Successive applications of just such phenol as adheres 
to the point only of a sharply serrated plugger are made, followed by 
slight scratching only so that blood shall not be drawn. By repeti- 
tions the bone is ultimately reached. 

A fresh drop of phenol is applied, the periosteum scraped away 
slightly, and the drill then used. 

A Rollins tubular knife (Fig. 505) has been used with success to 
remove a piece of gum, after which the drill or a fine trephine 
(Fig. 506) is used. Some acute pain may follow this operation, but 
usually lasts only a short time. 

Fig. 505 Fia. 506 




Tubular knives. 



Walker- Younger trephines. 



If antiseptics are used to syringe out the abscess cavity, it is better 
to use a mixture of six parts hamamelis (aqueous) and one part 
listerine as a partial sedative. The use of hydrogen dioxid is often 
very painful, owing to the rapid reaction with the blood present, and 
as it sometimes also drives the infective material into remote parts 
without disinfecting it, its use in this connection is not without 
danger, and should be avoided. 

It has been a subject of controversy whether a tooth should be 
extracted while the abscess is in the second stage. It has been 
claimed that the continuation of pus formation after extraction 
renders the state of the patient worse than before extracted. 

This occurrence is comparatively infrequently seen, and is, of 
course, due either to the retention of some pyogenic organisms 
34 



530 PERICEMENTITIS 

beneath the clot which forms in the alveolus or the infection of the 
parts by extraneous organisms. 

The retention of the tooth until a fistula forms would also confine 
the bacteria for the time. 

Unquestionably metastatic infections have appeared as the result 
of persistent local infection following tooth extraction, the avenue 
being the lymphatics or bloodvessels ; therefore, in cases of extraction 
during the second stage of pus formation apex of the alveolus should be 
curetted — syringed out with an antiseptic and a clot allowed to form. 
If it be thought desirable to repeat the syringing, a tent of antiseptic 
gauze may be gently carried to the apex of the alveolus and left. This 
tent may be removed to permit syringing, and should never be left long 
at any one time, as septic inflammation of the alveolar walls may occur. 
It also does not drain pus readily, so it might cause an abscess if 
left too long. (For curettes see Apicoectomy.) 

In cases of this kind oral sterilization and anti-infective systemic 
medication are of importance. As soon as improvement is noted the 
tent should be removed, the alveolus sterilized as before, and a new 
clot induced by a curetting of the walls. The case should now pro- 
ceed as any ordinary extraction; if not, it should be treated as for 
" dry socket ' ' (which see) . 

In a reply to a circular letter of questions regarding this point, 
Black, Kirk, Ottolengui, HorTheinz, and Schamburg all favored 
extraction as a means of removal of the cause and as a less evil than 
allowing the tooth to remain enclosing the bacteria, which, if cap- 
able of producing septicemia, it would do if allowed to remain. They 
are therefore in agreement with the editor's position taken in the 
second edition of this work (1904). Brown argues the difficulty of 
decision in an individual case. All are practically opposed to the 
idea that pneumonia is more likely to result from postextraction 
sepsis than septicemia, Morris 1 having taken the position that 
pneumonia resulted from extractions in this condition. Each and 
all advised careful ante- and postextraction antisepsis. 

The editor has had quite a number of cases of necrosis (necrotic 
dry socket) following extractions at the hands of specialists, and 
believes they and he should have been more watchful in these cases, 
and that in most cases a strong solution of potassium permanganate 
should be used as a wash before and after extraction, or tincture 
of iodin be locally applied, especially in cases requiring laceration 
of the gum. Antiseptic spraying of the alveolus, etc., is a reliable 
measure. In one case of extraction of a lower third molar opera- 

1 Mitchell: Dental Cosmos, 1907, p. 713. 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 531 

tion under anesthesia for prevention of progressive necrosis became 
necessary. The making of a cautious diagnosis and awaiting the 
proper time, as recommended by Mitchell, is a physical impossi- 
bility unless one await the third stage or a fistula or general infection, 
as in this state the bacteria are considered virulent, especially while 
bone solution is in progress. 

The Third Stage of Acute Apical Abscess. — In this stage the pus 
has found its way through or beneath the periosteum on the outside 
of the bone; therefore its germs are engaged in liquefying the gum 
tissue or in unusual location the mucosa or muscular tissue of the 
part. Except in these cases the gum is tumefied, a hard, circum- 
scribed, inflamed nodule indicating pus near the bone, or a soft, more 
generally diffused swelling indicating more superficially located pus, 
while a soft yellow or yellowish-pink tumefaction indicates pointing. 
In all these cases the indication is for a surgical opening of the gum 
rather than the opening of the tooth. The part should be gently 
disinfected with tincture of iodin or diluted Talbot's iodoglycerol on a 
ball of cotton, and a sharp bistoury should be boldly driven to the 
bone, with the cutting edge turned parallel with the alveolar bone. 
The lip or cheek is to be drawn well away to avoid injuring the coro- 
noid, buccal, or facial artery. A cut about a half to three-quarters 
of an inch in length is rapidly made by sweeping the edge and point 
occlusally. Too deep lancing upon the hard palate may injure the 
anterior palatine artery. 

As this is usually painful, it is better to refrigerate the gum with 
ethyl chlorid or operate under short general anesthesia, e. g., nitrous 
oxid, somnoform or the first impression of ether. Novocain is only 
useful in the case of deep-seated pus when injected into the more 
healthy tissue around the area to the opened, or as a means of con- 
ductive anesthesia. Next, the abscess tract is to be gently washed out 
with the hamamelis and listerine solution (see page 529), preferably 
warmed. Fairly hot water containing an antiseptic also gives relief. 

If the abscess has been deep-seated it is well to introduce a fine 
tent of antiseptic gauze through the opening into the abscess tract 
to prevent the too rapid healing of the external orifice which is apt 
to occur, owing to the approximation of the lips of the wound pro- 
duced by cheek pressure. This healing sometimes permits a second 
collection of pus. The tent should be removed not later than the 
next day, the abscess tract disinfected again, possibly with a mer- 
curic chlorid solution, and a new tent placed. The patient should 
always be cautioned to remove the tent if swelling return, as this 
indicates a stoppage of the vent, with collection of pus. At this time 
the tooth should be opened and disinfected if not tolerable at the 



532 PERICEMENTITIS 

first sitting. When this is tolerable the crown may be tapped and 
formocresol sealed in the pulp chamber, just before the operation of 
lancing, in order to permit disinfection and thus limit pus formation 
and to save time. 

When diffuse cellulitis with marked febrile disturbance passing 
into the adynamic type is produced, one should fear general infec- 
tion with virulent bacteria and treat not only locally, but use 
blood germicides against a possible septicemia. In these cases there 
may be little pus formed compared with the area involved. 

As a preventive of possible blood infection the following may be 
administered as a blood antiseptic and tonic: 

1$ — Hydrargyri bichloridi gr.j 

Tincturae ferri chloridi f5j — M. 

Sig. — Twenty drops in water four times a day. 

The editor employed this remedy with markedly beneficial effect, 
while suffering from a very severe abscess about the finger-nail, due 
to infection by the Streptococcus pyogenes and associated with 
lymphangitis extending as a bright red streak into the axilla. 

If the adynamia and other symptoms be progressive, medical 
cooperation should be obtained to divide the responsibility and to 
afford every means possible toward the cure. The extraction of the 
tooth followed by sterilization and curettement of the part, and the 
use of streptococcus antitoxin or vaccine conjoined with the 
sustention of the vital powers by nutritious predigested food and 
alcohol is logical. In even ordinarily severe cases not of this variety 
there will be some fever due to the toxin absorbed, and the pain, loss 
of sleep and appetite will cause physical debility. 

For this there is nothing better than the following, as tonic, anti- 
septic, and antipyretic: 

I*— Saloli, 

Quininse sulphatis (vel hydrochloratis) . . . . aa gr. lx 
M. et riant capsulas no. xx. 
Sig. — Take one four to six times daily, before meals when near them. 

Or, 

1$ — Quininae sulphatis gr. xxx 

Acetanilidi gr. xxiv 

Caffeinae citratis gr. iij 

M. et fiant pil. no. xij. 

Sig. — One every hour. (Endelmann.) 

The facial swelling resolves with the cure of the abscess or its proper 
venting, but may be assisted by cold applications or cataplasma 
kaolini to the outside of the face and by gentle massage by the 
patient or nurse. (See pages 526 and 533.) 



DISEASE OF PERICEMENTUM BEGINNING AT APEX 533 

As a means of reducing hard swellings vibratory massage is use- 
ful. A simple appliance for this purpose, devised by W. H. Mitchell, 1 
consists of a cam-like piece of metal perforated at its smaller end for 
mounting upon a screw mandril; it is held in the dental hand piece 
strapped to the hand as shown. Its centrifugal force imparts a 
vibratory motion to the hand which can be utilized for massage with 
the finger tips, or by holding in the hand an instrument containing 
upon its end a soft rubber cup. The part to be massaged should 
be lubricated with vaselin (Figs. 507 and 508). 



Fig. 507 



Fig. 508 




W. H. Mitchell's vibrator strapped to 
hand. 



W. H. Mitchell's vibrator and rubber 
cup applicator. 



The heat of a 100 candle electric lamp concentrated upon the face 
by a parabolic reflector from a short distance and followed by massage 
is also useful in facial swellings due to cellulitis. The high frequency 
current from a violet-ray apparatus is also useful, furnishing an 
electrical cell massage. 

Under no circumstances should hot poultices be applied to the 
outside of the face, as a discharge of pus in that direction will cause 
a disfiguring scar. If an abscess threaten to open externally, the 
abscess should be opened by an incision made from a point within 
the mouth, and, after sterilization of the tract, a drainage tent of 
antiseptic gauze should be introduced nearly to the bottom of the 
pus cavity. This should be removed daily, the abscess cavity steril- 
ized, and the tent renewed. An antiphlogistic compress should be 
applied to the face. The principal object sought is the mechanical 
apposition of the walls of the abscess cavity at the dependent or 



Dental Brief, 1908; Academy of Stomatology. 



534 PERICEMENTITIS 

external portion, in order that these shall unite by granulation and 
that the fistula shall in this manner become an ordinary one. The 
patient should lie in a position to counteract the natural effect of 
gravitation. 

After lancing, the mouth should be kept well sterilized by frequent 
sprays or gargles of hydrogen dioxid, which may be diluted to one- 
third strength with water — i. e., to a 1 per cent, solution. 

When the general periosteum is involved, as shown by extensive 
boggy swelling in the mouth, if several free incisions carried to the 
bone do not afford prompt relief, the tooth which is the center of 
infection should be promptly extracted. If, in the continued course 
of the pericementitis, chills, followed by fever, a coated tongue, and 
much physical depression occur, a general infection is to be feared, 
and no time should be lost in sterilizing the mouth, extracting the 
tooth, and subjecting the socket to free spraying with antiseptics. 
Systemic treatment is to be given (see pages 529 and 532). 

After-treatment. — The after treatment of acute apical abscess 
which has been relieved by abortion is exactly that of moist gangrene 
or of chronic abscess without fistula (which see). In very mild 
cases the formaldehyd treatment may be instituted at once. In 
severe cases it is better to allow drainage for a day or two. When 
the relief has been afforded by lancing the treatment is as for chronic 
abscess with a fistula (see page 541). 

One may not expect to find the bone immediately restored in 
either case. 

Acute septic apical pericementitis may occur on a temporary tooth, 
most frequently a temporary molar. The symptoms and pathology 
are the same, except that the looser character of the alveolar struc- 
ture seems to frequently permit the abscess to assume the chronic 
form before the dentist is consulted. Children often hide these 
conditions from their elders out of fear of the dentist. In strumous 
children the inflammation may be spreading and the lymphatic 
glands may be involved. There may also be some symptoms of 
septic intoxication evidenced by chills accompanied by fever, etc. 
These cases require an opening of the abscess, sterilization of the 
part, and attention to the systemic condition. If seen in the acute 
stage the treatment is the same as for the permanent teeth, unless 
the disease occur shortly before the date for eruption of the per- 
manent successor, when the temporary tooth should be extracted, 
If treated, the canals should be filled with materials which can be 
resorbed by the tissues, such as paraffin or wax with aristol, para- 
form, or thymol (Fig. 547). 



CHAPTER XVII. 
CHRONIC SEPTIC APICAL PERICEMENTITIS. 

Strictly this title refers to any long-continued septic inflammation 
of the apical tissue, but as nearly all such are due to continued infec- 
tion from the root canals we have the following varieties: 

1. When an acute abscess is aborted via the root canal or when 
open roots are infected and cause semi-acute or chronic abscesses 
which find some vent via the canal. 

This is known as chronic apical abscess discharging via the root 
canal (which in reality acts as a fistulous tract) . 

2. An acute apical abscess runs its active course and discharges in 
one of the described locations (see pages 518 to 523). This is known 
a chronic apical abscess with fistula. 

3. An abscess sac forms upon the end of a root having no vent or 
only partial vent and chronically persists without other discharge 
than a possible absorption of the pus into the blood. This may be 
of various grades and is called a chronic blind apical abscess. 

The apical granuloma (4) may also have a small abscess within it. 

4. The tissues react slowly to the infection and irritation, form a 
more or less dense granulation tissue which in its enlargement causes 
apical bone absorption. This growth is commonly known as a granu- 
loma, They are of several varieties as will be described later (p. 555). 
It may or may not contain pus cavities or may be cystic in character. 

CHRONIC APICAL ABSCESS DISCHARGING VIA THE 
ROOT CANAL. 

Pathology and Morbid Anatomy. — First Grade. — Upon abortion of 
an acute abscess in the first stage the pressure of pus upon the apical 
tissues is released, and, as a rule, the walls of the abscess cavity 
throw out granulations which fill it. This tissue tends to organize 
into more or less healthy tissue (cicatricial tissue). The bacteria 
are more or less killed out except at that part represented by imme- 
diate contact with the root foramen; at this point the tissues are 
infected and. some molecular loss of tissue as pus may occur. A 
limited loss of granulation tissue by pus formation is compensated for 

(535) 



536 CHRONIC SEPTIC APICAL PERICEMENTITIS 

by the formation of new granulations. The conditions are almost 
analogous to those existing in putrefaction of the pulp, and require 
analogous treatment. 

Second Grade. — If the abortion of the abscess has only partly 
permitted the pus to drain, or the alveolar walls or crypts of the 
abscess wall remain infected, the pus will continue to form and 
escape in some degree via the canal. If the tooth now be extracted, 
a small abscess sac will be found upon the root end. If opened, 
this will be seen to be a mass of fibrovascular tissue (inflamed peri- 
cemental apical tissue) having a central lumen connecting with the 
root canal (the abscess cavity). 

The so-called chronic blind apical abscess (3) does not differ from 
this pathologically except in having no outlet and it may be that the 
second and third grades may be intimately bound up with the granu- 
lomata. 

Third Grade. — With partial vent to the pus formed, the abscess 
cavity of the second grade may enlarge, involve the bony walls of 
the alveolus, and the soft tissues then pro- 
Fig. 509 liferate to such an extent that they finally 

organize into a large, fibrous, vascular sac 
attached to the tooth. This sac has the 
central pus cavity before described, which is 
connected with the pulp canal. It may be 
a half -inch or more in length (Fig. 509), 
and may be extracted with the tooth or 
may be left attached to the bone. It neces- 
sarily occupies in the latter a cavity of a size 
thi?d r ° g n rade a : Pi t llTcZ corresponding to its own bulk. As its inner 
sac containing a central walls are infected, extraction without its 
^otj^canai^con^afning removal leaves an infected area, which must 
pus. be disinfected or a secondary acute abscess 

may result. (See page 529.) One case which 
had given only slight uneasiness owing to partial vent, was treated 
at two o'clock and the tooth extracted at midnight, had the appear- 
ance shown in Fig. 509. 

Fourth Grade. — Instead of organizing, the fibrovascular tissue 
may be liquefied into pus or be liquefied after organization and bone 
resorption. The root apex becomes denuded for a distance about 
the apical foramen. Pus collects about the apex of the root and rests 
upon the bone, owing to the influence of gravity. The bone is thus 
infected, inflamed, and further liquefied, while necessarily the abscess 
cavity enlarges. If a bistoury be thrust through the labial alveolar 
wall in such a case, as shown in Fig. 510, but slight resistance will 




CHRONIC APICAL ABSCESS 



537 



need to be overcome. In the lower jaw the tendency is to burrow 
into the cancellated tissue of the bone away from the tooth, so that 



Fig. 510 



Fig. 511 




Chronic abscess on upper incisor, showing 
tendency of pus progressively to destroy peri- 
cementum, owing to the influence of gravity. 



Chronic abscess upon lower tooth 
showing tendency of pus to sink 
into the substance of the lower 
maxilla, owing to the influence of 
gravity. 



destruction of the pericementum may not be very extensive. In the 
upper jaw the tendency is to spread along the pericementum and into 
the cancellated bone, so that the cavities of chronic abscess upon 



Fig 512 



Fig. 513 





Chronic apical abscess discharging 
through the hard palate and threatening 
to discharge labially. 



Chronic abscess, showing de- 
nudation of apex of root (a to b), 
with deposits of calculi (a) upon 
cementum. 



the upper anterior teeth particularly may cause extensive excavation 
in the palatal process of the superior maxillary bone (Fig. 512). The 



538 



CHROXIC SEPTIC APICAL PERICEMENTITIS 



pus may burrow in irregular and circuitous directions until it finds 
external vent. 

In long-established cases deposits of pus calculi (serumal) may 
form upon the root end (Fig. 513). The cement corpuscles of the 
apical cementum may die and the root tissue itself become infected. 
In other cases resorption of the root end occurs. (See Resorption.) 

Symptoms. — In all of these cases the formations are gradual, owing 
to the partial vent or accommodation, and no pain beyond a slight 
gnawing or feeling of fulness or an occasional reflex pain may occur. 
If for any reason a vent become occluded, the pus formation may 
become rapid and an acute abscess is set up, which may be painful 
or not, according to the amount of tension produced before discharge 
of the pus. Aside from this, the gum color at the apex is somewhat 
deepened, the tooth is slightly loosened, and slightly tender to 
percussion. Signs of previous moist gangrene are in evidence. 

Diagnosis. — The passage, without production of sensation, of an 
undue length of fine probe into a canal is evidence of destruction of 
apical tissue and a guide to its probable extent. 

Fig. 514 




Central abscessed. Lateral as described in text, p. 501. Resorption of cuspid, 
looks like a perforation but due to lingual half of apical end being eaten out bj- 
resorption. All teeth extracted. 



A radiograph will show the area of bone destruction caused either 
by suppuration or resorption. This area may be largely filled with 
granulations a few days after abscess abortion or in the other various 
chronic abscesses or granulomata. The quantity of pus discharged 
at any one time is a fair guide to the size of the pus cavity, but a large 
bone cavity according to the radiograph may be lined with granu- 
lations or possibly it may be necrosed. In a few cases with fair 
foramina the end of the probe may produce sensation which is 
fair evidence that granulations have been formed and that living 
tissue is present. Talbot places a finger of the left hand over the 
suspected apical spaces and strikes the cusps with a heavy instru- 



CHRONIC APICAL ABSCESS 539 

inent at different angles, vibration of the left finger indicates a 
space. 1 

An extensively inflamed gum tissue over the apex indicates a 
probable approach of pus formation to gum tissue. The presence 
of pus in the canal or upon several dry cottons introduced for absorb- 
ent purposes is diagnostic of chronic apical abscess even though a 
granuloma is present 

If the probe encounters sensitive living tissue in the probable 
region of the apex and no pus can be found while yet a radiograph 
shows an area of apical bone destruction, a diagnosis of apical granu- 
loma is to be made. However, as both are infective conditions if a 
dressing be placed which shall not in itself be powerful enough to 
destroy the apical infection, a true acute apical abscess may super- 
vene. This, therefore, is not a diagnostic test (Figs. 515 and 543). 

A root cyst is sometimes diagnosable at once by its presence over a 
root. It is usually bluish about its margin with a clear stretched look 
in the center. It cannot be diagnosed as such by radiography but 
may be inferred when an area apparently circumscribed by bone 
shows. It should be treated surgically. (See Apicoectomy.) 

Treatment. — The first and second grades of chronic apical abscess 
discharging via the canal may be treated upon exactly the same 
principles which are involved in the treatment of moist gangrene 
of the pulp. The infection is considered as simply more deep seated, 
so that it is necessary to pass disinfectants into the abscess cavity 
with two objects in view: (1) To destroy the bacteria present; (2) 
to stimulate the tissues to granulative activity. The canal should be 
scraped and the foramen very slightly enlarged if necessary with a 
fine Donaldson cleanser, the canal having been flooded with 10 per 
cent, formalin or formocresol as an antiseptic. 

If necessary the root canal may be otherwise enlarged. (See 
page 497.) 

A dressing of 10 per cent, formalin or phenol-camphor to which a 
little menthol and a drop of formaldehyd, 40 per cent., have been 
added, or modified formocresol, should be loosely placed in the canal 
and the tooth sealed for twenty-four hours with cement, or, if the 
tooth has been very troublesome and is still tender, temporary 
stopping may be used and the patient provided with instruments 
suited to the removal of the covering and the cotton. It is better 
that the tooth should be under the control of the patient. At the 
next sitting the canal dressings are more tightly made unless the tooth 
is still sore when eugenol plus menthol or camphophenique plus 
menthol is to be placed in the canal — run down with a probe and 

1 Dental Cosmos, 1916, p. 727. 



.40 



CHRONIC SEPTIC APICAL PERICEMENTITIS 



Formocresol on cotton placed in the pulp cavity. The seal may still be 
temporary stopping if mastication has not proved destructive of the 
previous one. This is simply one method of treatment, other methods 
are to be found on page 491). When no pus can be found on the dress- 
ing or following it, or on an exploratory cotton twist, and there is no 
odor or pain, and if a culture proves negative (see page 503) the root 
may be filled; a temporary crown filling of gutta-percha should be 
used for a week or two. Each change of dressing should be done 
under aseptic precautions (see p. 448). 

In a relatively few cases teeth cannot be closed at all without a 
recurrence of trouble within a short period, which trouble is usually 
relieved by opening the tooth. The repetition of this is annoying, 
and in some cases is due to the strength of medicaments such as 
formaldehyd, which should be modified or abandoned for sedative 
antiseptics such as phenol-camphor or eugenol plus menthol or 



Fig. 515 



Fig. 516 





Abscess on tooth infected from mouth 
(see text.) 



The same as Fig. 515 (see text). 



an^aqueous medicament plus iodoform (see page 500). In some of 
the cases the gases may accumulate more rapidly than disinfec- 
tion occurs. In other cases the irritability of the tissues seems to 
produce intolerance of any remedial measures. What is known 
as "systematic stopping and unstopping" seems sometimes to over- 
come the irritability and accustom the tissues to being covered. 
The system consists of stopping with the appropriate germicide for 
about eight hours, or from morning to afternoon, then venting and 
redressing until the following morning, then for twenty-four hours, 
then forty-eight, then seventy-two, etc., until the tooth stays stopped. 
or in some cases the redressing may be done for several days con- 
secutively. Thus in one recent troublesome case three daily dressings 
of formocresol in the pulp chamber, then a Howe treatment with 
formocresol over it, followed by a similar treatment after forty-eight 
hours and a third after another forty-eight hours started the tooth 
on a comfortable progress. In the case shown in Figs. 515 and 516 



CHRONIC APICAL ABSCESS WITH FISTULA 541 

the crown was but a shell with caries even within the root. A com- 
bination of amalgam and cement plus thymol was placed over a cotton 
pellet in the root and before final hardening the filling was drilled 
through and the cotton removed. Formaldehyde was tried but 
pain ensued. It was treated with an aqueous solution and iodoform 
and finally filled. Pus was present for some time, later it disappeared. 

There have been a few patients who cannot seem to have teeth 
"treated," nearly all cases being practical failures even when aseptic 
Some few may be kept in comfort for a while with permanent vents, 
but this is objectionable, both from the oral sepsis and chronic apical 
abscess standpoint. In all troublesome cases persistently collecting 
pus at the apices and in all third and fourth grade cases, and trouble- 
some granulomata etc., an artificial fistula should be established and 
the case conducted accordingly. This is better and saves time. In 
some cases apicoectomy should be instituted at once after canal 
disinfection, instead of this intermediate treatment. 

In no case should hydrogen dioxid be forced in quantity into the 
pus occupying such an abscess cavity until the fistula has been made, 
and it is better even then to avoid it. It may bring about great pain, 
owing to the rapid reaction of the hydrogen dioxid with the pus and 
blood present. In some cases hydrogen dioxid has forced pus into 
remote locations without destroying it. As an adjuvant to abort 
acute suppurations of all sorts, Medalia 1 suggests the use of stock 
vaccines made of some 40 or 50 strains of Staphylococcus aureus 
and pneumococcus in the general average of 150 millions of former 
to 50 or 75 millions of the latter to the dose. (See Vaccines in 
Pyorrhoea.) 

Autogenous vaccines are used for the more persistent cases, the 
bacteria, of course, obtained from the pus of the abscess. 

CHRONIC APICAL ABSCESS WITH FISTULA. 

Morbid Anatomy and Pathology. — This form of chronic abscess 
occurs as the result of the discharge of an acute abscess through the 
gum or other part of the surface of the body, and whether the fistula 
has naturally occurred or been artificially established. (The interior 
of the mouth or other cavity exposed to contact with the air is 
considered external to the body proper.) 

If the acute abscess has been severe or long continued, the tissue 
destruction may be great, but, as a rule, granulation promptly sets 
in and the walls of the abscess cavity organize into cicatricial tissue. 
From the interior of this a canal (fistula or sinus) lined with cica- 

1 Dental Cosmos, January, 1914. 



542 



CHROXIC SEPTIC APICAL PERICEMENTITIS 



Fig. 517 



tricial tissue leads to the surface, the pus being almost constantly 
formed at the expense of the granulation tissue, which is as constantly 
renewed. 

The fistulous opening, as a rule, appears as a small teat of inflamed 
and sometimes pedunculated tissue located, in the majority of cases, 
upon the buccal surface of the gum, about a quarter of an inch below 
the apex of the root and slightly distal to it — a position probably 
determined by the density of the tissues surrounding the acute abscess. 

At times the only evidence of a fis- 
tula is a small spot of inflammation 
surrounding a minute opening, from 
which pus exudes. The fistula is 
sometimes located upon the lingual 
surface of the gum. It may per- 
forate the bone of the hard palate 
and open through the mucous mem- 
brane of the roof of the mouth (Fig. 
512). Instead of finding exit by a 
direct path through the buccal or 
lingual alveolar plate and gum, the 
pus may burrow along the length of 
the pericementum and discharge 
at the neck of the- tooth, and sim- 
ulate a pyorrhea pocket (Figs. 497 
and 498) . One-half or more of the 
lateral aspect of the pericementum 
may remain vital, although involved 
in a chronic inflammation, the re- 
mainder being destroyed. Not in- 
frequently the pus burrows along 
the surface of the bone and dis- 
charges at a point over an eden- 
tulous portion of the jaw. This is 
common to a lower bicuspid. It 
may burrow in the direction of 
the apices of other teeth, destroy their pulps and thus cause an 
abscess, having added causes for persistence. (See Acute Abscess, 
Class 5, p. 514.) 

When the apices of the roots of upper posterior teeth lie in very 
close proximity to the floor of the antrum, perforation of this floor 
may occur before tissue destruction has proceeded far enough in 
other directions to afford escape to the pus (Fig. 501). Extensive 
pus accumulations may occur in the antrum in consequence, and 




Chronic alveolar abscess of the root 
of a lower incisor, with abscess cavity 
passing through the body of the bone 
and discharging on the skin beneath 
the chin : a, very large abscess cavity ; 
b, mouth of the fistula. (Black.) 



CHRONIC APICAL ABSCESS WITH FISTULA 



543 



when the tissues in the antral floor are affected, other teeth may be 
involved. It may discharge into the nasal cavity, as a result of an 
acute abscess; at such points the discharge may remain persistent. 
Sometimes the discharge occurs through the canal of the affected 
tooth; the canal then acts as a fistula (Fig. 493). Upon a lower 



Fig. 518 



Fig. 519 




Fistula passing down through the body of 
the lower maxilla. (Black.) 

tooth, particularly the incisors, the 
pus may burrow downward through 
the cancellated tissue of the bone 
and emerge at the base of the bone 
and open upon the face (Fig. 518). 

In other cases the pus may per- 
forate the bone and find passage 
along the submuscular tissue, open- 
ing upon the face or neck (Fig. 
519). The apices of the roots of 
beneath the line of in- 




teeth lying 
sertion of 
may cause 



Chronic alveolar abscess at the 
root of a lower incisor, with a 
fistula discharging on the face under 
the chin: a, abscess cavity in the 
bone; b, b, b, fistula following in 
the periosteum down to the lower 
margin of the body of the bone and 
the mylohyoid muscle discharging on the skin. (Black.) 

an abscess to open in 
the neck cavity. Cryer records a case where an abscess opening 
upon the face immediately anterior to the line of the facial artery 
was traced to the root of a lower molar; the direction of the sinus 
is shown in Fig. 520. In a case having a similar anatomical associa- 
tion the pus penetrated the bone lingually, was encapsuled beneath 
the internal pterygoid muscle, and appeared as a swelling at the 
inner aspect of the angle of the jaw. Another case dissected along 
the muscles of the neck and discharged at the clavicle. Occasionally 
the apices of the roots of lower molars are separated from the inferior 
dental canal by only a thin lamina of bone, so that discharge into 
this canal may occur with infiltration along the vessels and nerves 



544 CHRONIC SEPTIC APICAL PERICEMENTITIS 

in the canal. Discharge into the nasal chamber is most frequently 
associated with abscess upon the upper incisors. 

Cementum infection occurs as a sequence to death of the cement 
corpuscles from lack of nutrition. Pus calculi may also form on the 
roots in the long continued cases. The granulation tissue springing 
up about the parts has a resorbent action and the root ends are 
often resorbed, though this action is probably to an extent counter- 
acted by the alkalinity of the pus. The formation of the latter may 
however be in abeyance at times. In certain areas hypercementosis 
may occur. A comprehension of these effects may be best obtained 
by the consideration of granulomata which to the mind of the writer 
represents that form of living resistant tissue which in its active form 
is capable of hypercemental construction or resorption and in its 
degenerative form produces cysts, abscess, etc. (see Fig. 539). 

The extent of tissue destruction varies considerably, but is usually 
greatest in dependent parts, gravity influencing the burrowing of 
the pus. 

Symptoms and Diagnosis. — A fistula is seen upon the gum, visible 
as either a small teat of flesh (perhaps pedunculated), discharging 
pus, or as a tiny orifice in the gum surrounded by inflamed tissue, 
and from which pus may be squeezed (Fig. 500). As a rule, a soft 
silver probe may be passed to the apex of a nearby root, whether 
possessing a crown or embedded in the bone (Fig. 307). In case of an 
external opening upon the face a similar procedure shows the trouble 
to lie with some tooth root. The x-rays will often be valuable in 
determining the exact location of the abscess cavity, but as a rule a 
fistulous tract does not show well in a radiograph. 

Upon the teeth themselves but four conditions may cause a fist- 
lous opening: (1) Putrefaction of the pulp or its equivalent apical 
infection; sometimes the sinus is at the oral end of a broken root; 
(2) septic perforations, apical or lateral; (3) a pericemental abscess 
(see Pericemental Abscess); or a secondary abscess associated with 
a pyorrhea pocket (see Pyorrhea Alveolaris); (4) lateral abscess 
about a third molar or impacted tooth. 

Aside from these, the probe may lead to carious or necrosed bone, 
a cyst, or a subperiosteal abscess (maxillary periostitis). 

In these cases the probe does not lead to a root. Carious bone 
will impart a honey-combed sensation to an excavator; necrosed 
bone will be exposed and firm, or the sequestrum will be in evidence 
as a movable body. There may also be several fistuke and extensive 
inflammation of the tissue. A cyst will be a tumor with certain 
characteristics (see page 187), and an impacted tooth will usually im- 
part the feel of smooth enamel to the instrument, though the enamel 



CHRONIC APICAL ABSCESS WITH FISTULA 



545 



may at times be rough at certain points. An embedded root will be 
movable, and will present the dentin and its central opening, the pulp 
canal, as diagnostic features. It may require radiography for deter- 
mination. Maxillary periostitis will, as a rule, have a history of 
traumatism, or the previous use of a probably infected hypodermic 
needle associated with it. In all cases not clearlv due to other than 



Fig. 520 



Fig. 521 




Abscess with tortuous sinus, open- 
ing upon the face: A, tissue of cheek; 
B, floor of mouth; G\ abscess tract. 

Fig. 522 





Large abscess cavity in relation with a 
lateral incisor, complicated by an im- 
pacted supernumerary tooth beneath the 
nasal spine. (Philadelphia Dental College 
Museum.) 



dental causes, evidence of the four 
dental conditions mentioned should 
be sought. 

A chronic abscess with fistula 

occasionally heals at the orifice and 

may break out again. This shows 

a spontaneous return to a blind 

abscess. For this reason in any case of apparent cure by root filling, 

etc., a radiograph should be taken at varying periods to determine a 

real cure. 

Treatment. — Necrosed, or carious bone, abscesses or perforations 
and pericemental abscesses will be treated of under proper headings. 
Here only chronic apical abscess with fistula will be discussed. 

In the cases due to moist gangrene of the pulp the canals must be 
35 



Abscess and resorption at apex. 
(Radiograph by Lodge.) 



546 CHRONIC SEPTIC APICAL PERICEMENTITIS 

freely entered, the apical foramen opened with Donaldson or other 
cleansers, and the canals and abscess tract thoroughly sterilized. 

Owing to the complexities of most roots the following procedure 
seems necessary. The pulp cavity and coronal portion of canals are 
prepared for easy entrance and the apical portions gently syringed 
out while agitated with a fine broach. As the case is one of pulp 
putrefaction, no unnecessary force should be used. 

The canals are now dried and a formocresol dressing introduced 
into the pulp cavity only and tightly sealed with cement or temporary 
stopping. (See pages 495 and 498.) 

A radiograph is made before dismissal which is developed before the 
next sitting or the patient is referred to a radiographer for the same. 

With this as a guide, the non-fistulous root is treated as for simple 
putrefactive pulp (it being possible to excite an abscess on it), but the 
fistulous root is made continuous with the abscess tract. Formocresol 
or phenolsulphonic acid 1 or 10 per cent, aqueous formaldehyd may 
be in the canal while working upon it. A thread of cotton with strong 
phenol is to be packed in the fistulous canal and pressure with raw 
vulcanite or gutta-percha made on this cotton only to force the 
phenol through the fistula, which may be prevented from burning the 
mouth by holding a bit of cottonoid roll over the fistula. The escharo- 
tic effect is valuable. Hydrogen dioxid, or antiseptic liquid soap or 
Talbot's iodoglycerol may be used if preferred. Phenolsulphonic 
acid may be used. 

The non-fistulous canals are to be treated with formaldehyde 
dressings on cotton gently placed. These dressings are renewed with 
formocresol until sterility is certain (see page 503) and the abscess 
healed. 

The nozzle of a hypodermic needle may be fitted to the canal by 
packing wax, temporary stopping, or raw vulcanite about it; a piece 
of flexible tubing may be previously stretched over the free end 
and the other end of the tubing stripped over the compressed-air 
syringe. Medicaments or air may thus be blown through the fistula. 
Instead an abscess syringe, filled with an antiseptic, may be used in 
like manner. The method should be cautiously used in fistulous 
cases only, except for reasons well known by the operators employing 
them, as very painful distention of the cheek may occur. (See p. 504.) 

The rubber cup shown in Fig. 526 may be used as a vacuum pump 

1 Phenolsulphonic acid consists of 97 parts, by weight, of concentrated sulphuric 
acid and 93 parts, by weight, of phenol, kept at 100° C. for about twenty-four hours 
to produce a reaction, when sufficient distilled water is added to make the liquid 
assay about 80 per cent. -of phenolsulphonic acid. (Buckley, Lilly.) Prinz, in Cosmos, 
April, 1912, gives some good reasons for its inferiority for any purpose to sulphuric 
acid, though Buckley has shown good results from its use in chronic apical infections. 



CHRONIC APICAL ABSCESS WITH FISTULA 547 

Fig. 523 F IG . 524 

O 



1 :il! 





Minim syringe. 



J. N. Farrar's alveolar abscess syringe. 



Fig. 525 




Bulb syringe. (Berlin.) 



548 



CHRONIC SEPTIC APICAL PERICEMENTITIS 



to draw the pus from the fistula or to draw medicaments through 
the canals. If modified by introducing a glass tube and connecting 
this up with a rubber bulb the saliva ejector tube, an aspirator pump, 
or with the intake of an air compressing pump a vacuum device of any 
force desired may be obtained. As a rule, the first method will work 
if any of them will, and saves time. 

Opening the fistula daily with a probe or needle or a piece of iron 
stovepipe wire aids healing from the bottom out. This may be done 
by the patient. 

Tissues about abscesses have an inherent tendency to repair; cases 
of long standing frequently healing promptly, sometimes, though not 
often, in twenty-four hours. 1 



Fig. 526 



Fig. 527 





Rubber cup to be used as a 
vacuum cup. 



Amputation of root apex: OG, opening in 
the gum made by packing fistula; AC, 
abscess cavity; RF, root filling. 



In indolent chronic inflammation the use of a small gum dry 
cup with vacuum bulb attached may be used for a few minutes 
at a time several times a day, to draw fresh blood and effusions 
into the inflamed part. The opsonic index of the lymph drawn 
in is said to be raised to several times beyond that of the body lymph, 
thus rapidly increasing phagocytosis in the part. The rubber cup 
shown in Fig. 526 may be left imperforate and furnished the patient 
for this purpose. 

If the abscess cavity does not heal in a week or two one of several 
causes may be assigned: (1) The crypts in the walls of the abscess 
cavity may require further disinfection. If improving, the treatments 
are continued or the phenol, etc., forcing be repeated, or the Howe 
treatment applied. (2) The cotton in the canal may have absorbed 

1 Darby, Proceedings of Academy of Stomatology, Philadelphia, 1899. 



CHRONIC APICAL ABSCESS WITH FISTULA 



549 



pus formed after an interval of antiseptic influence and may keep 
up the infection. This calls for a non-absorbent dressing or imme- 
diate root filling-, after say, an hour of formocresol application or the 
Howe treatment. (3) The root canai may not be explorable, in 
which case the Howe silver nitrate method may be employed at once 
on finding such condition. Apicoectomy may finally be required, or, 
if feasible, performed early. (See Apicoectomy.) (4) The root end 
may be encrusted with calculus, or the cementum be infected, or dead 
bone may be present. 



Fig. 528 



Fig. 529 



Fig. 530 






A skiagraph of apical 
abscess cavity about two 
root apices; incurable 
by ordinary means. 



The same after root 
amputation. 



The same thirty 
days later, showing 
a certain amount of 
new bone formation. 
(Price.) 



For these cases the apical foramen should be sealed and the abscess 
tract syringed once a week with 25 per cent, sulphuric acid, the 
mouth and clothing being properly protected by using a pad of cot- 
tonoid over the fistula and needle to absorb the excess. This dissolves 
calculi and disinfects dead cementum. It also stimulates the soft 
parts to a granulative action. If necessary the patient should receive 
appropriate systemic treatment, especially if anemic. (See page 558.) 
In this way some old and somewhat obstinate cases may be induced 
to heal. In some cases gravity so retains pus in abscess cavities that 
granulation is interfered with. The instruction of the patient in the 
syringing out of the tract with a mild antiseptic several times a day 
is of great value in that it removes pus which if retained would destroy 
granulations. Hydrogen dioxid should not be used except in small 
abscesses as it may cause the forcing of pus to distant areas. Many 
apparently desperate cases heal of their own accord after some months. 
Some success attends the packing of a root with a thick paste of 
iodoform after opening the root as far as possible (see p. 476). 
Cases in which a canal was not explorable for any considerable dis- 



550 CHRONTC SEPTIC APICAL PERICEMENTITIS 

tance have healed after this treatment. The .x-ray application, made 
for ten or twenty seconds, or skiagraphy seems to aid the healing of 
the fistula. The high frequency current also is a stimulant. A metal 
probe is introduced into the fistula and the violet-ray electrode held 
in contact with it. If the abscess be incurable by the above methods 
or radical measures being considered better, without attempting con- 
servative measures, the root end may be amputated, after a tight 
canal filling is placed beyond the point at which amputation is to be 
done. From the standpoint of the possible eventual incurability or 
apparent cure with a pathological condition still possible, it is a 
saving of time to go at once to apicoectomy root amputation 
or replantation. The methods are discussed in special chapters in 
this work. 

Necrosed root ends may occasionally be seen projecting through 
the gum and alveolar process which have been lost above them. 
They should be removed as above indicated. Sometimes salivary 
calculus deposit* on them. 

Perforations. — A septic perforation may occur in the course of 
opening septic root canals. As a rule, the canal being difficult at 
first, it cannot be opened after perforation because the probe con- 
tinually follows the false opening. If it can be done by better care, 
aided by radiography, the perforation is usually near the crown and 
can sometimes be filled with gutta-percha and eliminated. 

In a few cases under local anesthesia one may cut down through 
the gum upon the perforation, pack the tissue once or twice with 
cotton and sandarac plus orthoform and cut out the perforation into 
a cavity and fill with amalgam. Again packing, the amalgam is 
smoothed the following day. A probe should be put into the canal 
while filling to maintain the canal lumen. Perforations well up 
toward the apex call for apicoectomy or replantation (which 
see) or extraction as they cannot be filled without leaving septic 
root ends. 

Several cases of fistulous openings into the antrum have been 
noted by canal exploration in which no history of discomfort from 
antral empyema could be obtained. It was assumed that the root 
ends approximated the floor of the antrum, and that the abscesses 
were of simple chronic type. Such cases were treated upon the 
common principle of canal antisepsis, flushing the abscess tract 
with an antiseptic, and filling the canals. The antral condition 
was explained to the patients, who were warned of possibilities, but 
such as yet have not been reported. 

A chronic abscess may discharge into the maxillary sinus for a 
long period before being discovered, unless the pus accumulation be 



CHRONIC APICAL ABSCESS WITH FISTULA 551 

extensive, when it escapes from the antrum into the cavity of the 
nose, discharging by one side. Smaller accumulations of pus find 
exit in the recumbent position, and attention is called to one antrum 
as the seat of affection by noting that in the morning pus or an 
offensive secretion appears at but one nostril. The patient complains 
of fulness upon lying on the affected side and is relieved by lying on 
the opposite side. The surgeon may note it upon examination or 
upon suction at the ostium maxillae (Brown). Brown notes pain 
over the side of the face even extending to the frontal, temporal and 
occipital regions, tenderness on pressure, hyperesthetic skin, neuralgia 
and tic douloureux; in rare cases bulging of the buccal antral wall 
with yielding and crepitation on pressure, thinning and bulging of 
the palatal wall in chronic cases. The discharges from purulent 
nasal catarrh appear upon both sides. 

High transillumination of the tissues about the mouth and through 
the cheek, by means of the electric mouth lamp of 20 volts capacity, 
the patient being in a dark room or both operator and patient under 
a spreading dark cloth, may reveal an opacity on one or perhaps both 
sides, indicating the presence of fluid in the antrum. A clear pinkish 
transillumination is a sign of health. Tumors in the antrum entirely 
obstruct the light. Examination of the posterior teeth will show one 
of them to be pulpless, if the cause lie in apical abscess. If such a 
tooth be extracted, a profuse flow of pus may follow, and a probe may 
be passed through an alveolus directly into the antrum. 

The diagnosis may be assisted by x-rstys, both antra being radio- 
graphed for comparison. Raper 1 states that the shadow does not 
actually demonstrate the presence of pus, but that something abnor- 
mal exists whether pus or a soft tumorous growth, the appearance 
being the same. It, however, locates the disease, whether in the 
antrum or other sinuses. The presence of opaque foreign bodies, 
as a piece of tooth root causing disease, is shown by radio- 
graphy. 

The teeth should be radiographed for abscess, etc.; when due to a 
tooth extraction is the best surgical relief. 

The nozzle of an atomizer or syringe, filled with a mild antiseptic 
solution, is passed into the antrum and the cavity is freely sprayed. 
A probe or the finger is passed into the cavity and an exploration 
made to detect the presence of any dead bone or bony septi, which, 
if found, must be removed, the cavity of entrance being enlarged 
to permit their removal. The antrum is then packed with gauze 
impregnated with iodoform, etc. After a few days the cavity is 

1 Items of Interest, July, 1912. 



,),)! 



CHROXIC SEPTIC APICAL PERICEMENTITIS 



sprayed about every other day with warm DobeH's solution, very 
dilute iodoglycerol, Lugol's solution, or sterile ocean water. 

In one case in which the writer opened into the antrum while 
curetting an alveolus necrotic from pyorrhea, a wide opening was made 
for exploration in the morning, and a small vulcanite plate with a 

Fig. 531 




A, antrum with pus in it. B, healthy antrum. (Radiograph by Carmen of St. Louis.) 
Courtesy of Dr. Howard R. Raper. 



solid upright plug constructed and inserted in the afternoon. The 
firm clot found was indented by the plug, but did not dissolve. The 
plug was cut down gradually and the part healed by organization of 
the original clot. The antrum was not diseased. This shows the 
inherent tendency to heal. 



CHRONIC APICAL ABSCESS WITH FISTULA 



553 



Fig. 532 



Iii any case of antral empyema due to apical abscess, the tooth 
may be extracted, the socket enlarged freely as above, and otherwise 
the case treated in the same manner or a drainage tube temporarily 
substituted for the plug. Tt might 
be converted into a plug to be cut 
down later. Other methods of 
treating antral empyema are em- 
ployed. (See works on Oral Sur- 
gery.) 

Unless necrosis of bone occur, 
cases of fistula opening upon the 
face or neck may be healed by the 
ordinary methods of canal treat- 
ment, carried out with extraordi- 
nary care to accomplish the irriga- 
tion of the fistula, or at least steri- 
lize the apical tissue. The scar 
formation is less than when extrac- 
tion is practised for the removal of the cause. If the fistula be 
indolent, the granulations may be stimulated by means of an 
injection of 10 per cent, silver nitrate solution. If the fistula 




Emypema of antrum due tc 
abscess upon root of bicuspid tooth. 
(Radiograph by Price.) 



Fig. 533 



Fig. 534 





Scar caused by alveolar abscess dis- 
charging on the face. (Black.) 



Operation for the remedy of scar on the face 
caused by alveolar abscess. (Black.) 



obstinately refuse to heal, the tooth should be extracted and necrosed 
bone, if any be present, surgically removed, though apicoectomy may 
be tried. 



554 CIIROXIC SEPTIC APICAL PERICEMENTITIS 

Flagg 1 suggested, as a means of lessening scar formation, that a 
seton be passed through the external fistula into the mouth, and that 
it be gradually drawn into the mouth as the external fistula heals, 
after which the tooth is to be extracted if otherwise incurable. 

In fistulse discharging upon the face the formation of scar tissue 
may bind the tissue of the cheek tight to the bone. When this 
occurs beneath the tip of the chin, the scar, after healing, usually 
resembles a dimple, and calls for no interference. The scar and 
binding down along the border of the inferior maxilla, or beneath 
the malar bone in the upper maxilla, may produce deformity calling 
for remedy (Figs. 533 and 534). Black's operation is to be performed 
to lessen the deformity, for its complete correction is not practicable. 
A finger placed in the mouth draws the cheek away from the alveolar 
wall, when the exact position of the cord of attachment is discovered. 
A tenotome knife is passed into the tissues, dividing the band of 
attachment; a long pin is passed through the most depressed portion 
of the scar, its center, the long ends of the pin resting upon the 
face; strips of adhesive plaster laid upon the skin under the head 
and point of the pin will prevent the latter sinking into the soft 
tissues. The pin is retained for several days, until the cut in the 
mouth heals. The principle involved is the supplying of a new 
section of scar tissue which, while it shrinks, makes the total length 
of the cord greater, hence less binding. 

Systemic Complications. — The cachectic, debilitated, anemic, tuber- 
culous, and syphilitic are liable to extensive pus formation, which 
enlarges the cavity unduly and may involve the roots of other 
teeth or even cause devitalization of their pulps, which aids in the 
continuance of the abscess by adding a fresh cause. 

In such cases all the dead pulps should be removed after careful 
diagnosis, and the patient should be instructed in the use of a Sub. 
Q. or Berlin syringe and a mild antiseptic, the object being to keep 
the dependent parts free of pus and allow granulations to form rather 
than be constantly broken down. In such cases hydrogen dioxid 
should be avoided as it may force undestroyed bacteria into remote 
parts. 

In addition, such systemic medication or remedial measures as 
will raise the recuperative and resistant powers of the tissues should 
be employed. The application of these is to be conducted by a con- 
sultant physician. 

If very persistent, a vaccine may be employed, after the method 
of Wright, to raise the opsonic index or Medalia's method of using 

1 Lectures on Dental Therapeutics. 



CHRONIC BLIND APICAL ABSCESS 555 

stock vaccines of known source may be employed (see index). 
The direct results of infection, toxemic and septicemic, have already 
been considered. Grieves contends that many root ends remain 
necrotic and develop blind abscesses and their sequela? (which see). 

Chronic Blind Apical Abscess. — A true blind abscess is one with- 
out a point of discharge. It is a result of septic contamination 
from root canals, a condition in which bacteria in unfilled root 
apices or in the interspaces between a root filling and the canal 
wall find their way into the fluid entering such a space and produce 
putrefaction — a condition practically analogous to moist gangrene 
of the pulp; or else bacteria in the blood arising from some other 
source, dental, tonsillar, or other focus, or entering to form a general 
blood infection, enter an apical region previously weakened as by 
pulp removal, apical irritation by root canal filling, a previous abscess, 
etc., and develop a chronic apical abscess. 

An apical abscess is formed and the apical tissue acts as a fibro- 
vascular envelope or sac. Under the pus pressure and the pumping 
force of masticatory movement, absorption of toxins and pus germs 
by way of the lymphatics occurs. The lymphatic glands may be 
involved; a systemic infection occurs. It is differentiated from 
granuloma by a discharge of pus on opening the root apex. It is 
treated as is an abscess discharging via the canal. (See p. 535.) 

Granuloma. — Under conditions of low grade irritation by the gases, 
toxic substances and bacteria of low virulence in root canals, contain- 
ing dead pulp, imperfect root fillings, etc., the apical tissue develops 
into a more or less solid mass of soft tissue. This mass of tissue is 
larger than the original apical space, as a rule, hence it represents an 
enlargement of apical tissue and must and does lie in an enlarged 
space in the bone corresponding to the size of the granuloma. Though 
its enlargement may remove the overlying bone this is due to bone 
resorption. Examination of these growths have shown that a pus 
cavity is only found in the later stages of comparatively few and these 
then may be the source of chronic blind apical abscess if continued, 
or, if they suddenly become active, may institute acute apical abscess 
or subacute apical abscess, meaning by the latter that form of abscess 
which causes cold abscess or a fistula without production of pain 
such as occurs in acute apical abscess, as a rule, or may produce 
occasional irritations which subside. 

Pathohistology. — The more recent and accessible work on this 
subject has been done by Thoma, 1 Hartzell and Henrici 2 , Dewey, 3 

1 Jour. Nat. Dent. Assn., October, 1917. 

2 Dental Cosmos, January, 1918. 

3 Ibid., July, 1918. 



556 CHRONIC SEPTIC APICAL PERICEMENTITIS 

Eisen and Ivy, 1 -and Endelman, 3 who, however, claim no originality 
and who are mentioned, to exclusion of others, simply for the value 
of their demonstrative work and easy accessibility. These writers 
are agreed that the growth consists of an exterior fibrous capsule 
continuous at the sides of the root apex with the pericementum (and 
probably consists of the proliferated pericemental fibers. — Ed.) and 
it extends into the trabecula? of bone. Its interior or central portion 
consists of delicate connective tissue filled with plasma cells (cells 
oval in form, with single excentrically situated nucleus, the cyto- 
plasm taking basic stain and regarded by Hartzell and Henrici as 
characteristic of chronic inflammation) arid containing bloodvessels. 

Touching this histology and the name, the following definition of 
a granuloma is taken from Hertzler's "Treatise on Tumors," a work 
not related to dentistry: " A tumorous enlargement and a structural 
resemblance to the newly formed tissue of wound healing." The term 
is applied by Hertzler to gumma and other infectious growths of 
chronic inflammatory character and seems fairly applicable to the 
dental condition. So far what is termed a "simple granuloma" has 
been described. Certain degenerative changes may occur in the 
central tissue. 

The stimulation may cause a proliferation of the natural epithelial 
cells of the part (variously called epithelial root sheath of Hertwig, 
epithelial debris of Malassez, glands of Black, or remains of enamel 
organ), " producing an epithelial mass which breads down in the 
center, it is believed, by fatty degeneration and a space is formed 
containing a fluid." This produces an epithelium-lined cavity, known 
as a paradental or peri-apical cyst (Fig. 541). The fluid may contain 
cholesterin crystals, which may in some cases appear in quantity 
(Fig. 541). The fatty degenerated tissue may be thickened into a 
pultaceous mass, known as caseation, and if a pus cavity is formed 
is the chronic blind abscess described on page 555. 

Calculus has been found in the center of the granuloma, probably 
due to fatty degeneration. 4 Certain effects of chronic inflammation 
are noted, i. e., root resorption and hypercementosis, which are 
regarded by the writer as effects of such chronic non-septic inflamma- 
tion or hyperemia as may be present (even though the central cause 
is infective). Necrosis of the osteoblasts in the cementum producing 
a necrotic root end is the natural result of any loss of attachment or 
infection reaching them. This is held by many as rendeiing the 
pericementum incapable of normal reattachment and as indicating 
necessity for apicoectomy when possible. 

1 Dental Items of Interest, February, 1916 - Ibid., p. 88. 

3 Dental Cosmos. November, 1917. * Hartzell and Henrici. 



GRANULOMA ABSCESS 



557 



Bacteriology. — Hartzell and Henrici usually found the root cysts 
and granulomas infected, and regard the Streptococcus viridans as 
the cause of the non-suppurative lesion and state that when pus is 
present the staphylococci, especially the S. albus is present. 1 





Fig. 535 






^r^ 


• 


^' 







Fig. 536 




Acute abscess, not shown in radio- 
graph. Two-rooted second bicuspid. 



Apical infections. Case of arthritis 
much improved after extraction. 



Endelman has shown that when these sacs (or chronic abscess) 
were implanted in culture media without disturbing them, no growth 
occurred in several instances, while their contents produced abundant 
growth. This would seem to show a tendency to circum valla t ion 
and resistance to infection, which may, however, be broken down. 
This fact, taken with extension of inflammatory elements outside the 
capsule, show the bone to be probably aseptically absorbed (Fig. 542). 



Fig. 537 



Fig. 538 





Case of septic pericementitis. Root 
hollowed out and perforated by caries. 
Fungous gum in root. 



Granulomas on bicuspid and both 
roots of first molar. 



Systemic Complications. — There is still work to be done to settle 
the question as to how far granuloma and chronic blind abscess may 
be considered dangerous. It is claimed by Rosenow and others that 
these are the most frequent cause of arthritis, endocarditis, muscular 
rheumatism, distant abscesses, etc., though any other foci of infection 



1 Hartzell and Henrici, p. II 



558 



CHRONIC SEPTIC APICAL PERICEMENTITIS 



such as in pyorrhea pockets, the tonsils, nasal sinuses, appendix 
vermiformis, etc., may also act to produce these conditions. The 
following possibilities of effects are grouped by Grieves: 1 



Fig. 539 




Root with granuloma, showing resorption of root; pulp necrosed. Inflammatory 
granulation tissue. (Thoma.) 

Fig. 540 




Photomicrograph of cross-section of granuloma removed by apicoectomy. Note epi- 
thelial lining in the center of the lesion. (Thoma.) 

1. Upon the muscles, causing myositis. 

2. Upon the joints, causing arthritis, synovitis, etc. 

3. Upon the blood, causing septic and pernicious anemia and 
endocarditis or pleurisy. 

4. Upon the glands, causing lymphadenitis. 



Dental Cosmos, May, 1914, p. 568. 



GRANULOMA 559 

5. Upon the nervous system, causing toxic neuritis and degenera- 
tion. 

6. Upon the organs of excretion, causing skin rashes and nephritis. 

7. Upon the gastro-intestinal tract, causing septic gastritis, enter- 
itis, cholecystitis, appendicitis, colitis, etc., and their sequelae. 

In the kidney lesions, Hartzell notes albuminuria and casts in 
quantity, lessening as the local foci of pus formations are removed. 1 

The symptom-complex 2 is mainly an anemic, pasty complexion, 
malaise, loss of appetite, debility, night sweats, loss of weight, low 
fever (100°), or subnormal temperature. 

Fig. 541 




Granuloma with capsule; epithelial proliferation, lining cystic cavity cholesterin crystals. 

(Thoma.) 

The abscesses are within the bone of the jaw while the dental 
symptoms may not be noticeable though the tooth may be slightly 
tender and there may be tenderness upon pressure over the apical 
region. There may be pain about the eyes or in the back of the head 
or neck. The postcervical glands may be enlarged. The fact 
that teeth have apparently been attended to is no warrant that 
septic conditions are not present, these conditions embracing any 
form of gingivitis or of pericemental infection, including pyorrhea. 

1 Journal of Allied Societies, June, 1914. 

2 Dental Cosmos, May, 1914, p. 569. 



560 CHRONIC SEPTIC APICAL PERICEMENTITIS 

Experiments by Hartzell in animals in an endeavor to produce sys- 
temic lesions, such as abscess of the kidney, were successful, but the 
chief evidence adduced of connection between apical granulomata and 
systemic disease is the frequent recovery of patients after the granu- 
lomas were removed, though when the extra-oral disease is well 
implanted, there is no absolute reason why it should not continue the 
infection on its own account and require other methods of treatment. 
Not infrequently cases of granuloma are complicated by the presence 
of pyorrhea alveolaris, or other conditions of' sepsis, such as filthy 
bridges, abundant calculus, etc., and there is still left the task of 
grouping the symptoms accompanying each class of cause. 

A Fig. 542 




Section showing that the capsule does not always mark the boundaries of the abscess. 
Chronic dento-alveolar abscesses are frequently trabeculated, two or more compart- 
ments entering into the formation of one so-called abscess sac. A. Fibrous capsule; 
B, Inflammatory elements which make up bulk of abscess; C, Inflammatory tissue 
reaction outside capsule. (Endelman.) 

In the main pyorrheal conditions and abscess with sinus are first 
apt to disturb the digestive tract, causing indigestion, intestinal 
putrefaction, toxemia and their malnutritional sequelae, while blind 
abscess and granuloma are more likely to produce the conditions due to 
direct transmission of infection via the blood stream (see the classifica- 
tion by Grieves, page 558) . Pyorrhea, etc., if permitting absorption of 
bacteria at the pocket might produce the same conditions as the granu- 
lomas. Many persons seem absolutely well in spite of the presence of 



GRANULOMA 561 

peri-apical infection, this being considered due to systemic resistance 
liable to break down when most required during some period of 
greater stress as an illness from some other cause, overwork, etc. 

The granuloma, etc., being in vascular relations and being always 
infected, the infection may be transferred to the blood and the 
bacteria locate wheresoever they will and in the new location 
produce the subacute, non-purulent inflammatory conditions know a 
as myositis, arthritis, etc. Rosenow concludes from experiments that 
these bacteria have selective affinity for parts to which they are 
accustomed. Thus in many cases, those taken from an appendix 
have selective affinity for the appendix of the experimental animal. 

In this connection, in a lecture, Price 1 demonstrated a case of severe 
wry-neck, due to a diseased tooth. A piece of cervical muscle contained 
the same bacteria as the dental region and the ground muscle injected 
into rabbits produced characteristic wry-neck in them. 

It is considered that the non-pyogenic streptococci are the main 
bacteria concerned. The toxins having affinity for cells also produce 
disease and symptoms. 

Diagnosis. — Every discolored or sore tooth should be suspected and 
radiographed unless test shows it thoroughly vital (see p. 483). The 
presence of a defined dark area in the negative (film) at the apex, 
together with no root filling or apparently imperfect filling is war- 
rant for opening the root canal and establishing a connection between 
canal and granuloma. If pus flows it is a case of chronic abscess, if 
none, it is considered granuloma. 

Treatment. — Upon finding the pulp dead or upon removing a partial 
root filling, the writer prefers to ignore the differential diagnosis, 
places formocresol for twenty-four hours and proceeds as in cases of 
pulp putrefaction (see p. 493). This is done because of the danger 
of acute abscess being set up by exploration at the first sitting. 
This form of treatment is best in cases of granuloma uncomplicated 
by systemic conditions. In case such are noted no matter how mild, 
and nearly every patient will complain of something, a neuritis, 
mild attacks of rheumatism, indigestion, bilious attacks, headaches, 
neuralgia, nervousness, debility, a previous breakdown, etc., both 
granuloma, etc., and gingival disorders should be looked for, the 
probable relation explained and thorough treatment advised. This 
is a matter of conscience with the dentists as the patient will have 
no knowledge, as a rule, of the relation. In severe systemic disorders 
either the teeth and mouth may be considered first, but often is the 
last examined area because other possibilities are excluded. 

1 Lecture before the Pennsylvania Slate and other Societies, ID 17. 

36 



562 



CHRONIC SEPTIC APICAL PERICEMENTITIS 



Radiography of the entire denture or at least of suspected areas 
picked out by a discriminating dentist should be done. In severe 
systemic complications extraction or root amputation is imperative 
for the reason that other methods are less certain of eradicating the 
focal infection. Naturally extraction is preferred in posterior teeth. 

In either case the granuloma should be removed and the bone 
curetted and a clot allowed to form, as a rule (see Apicoectomy) . 
The reason for rapid eradication is that treatment via canal is depen- 
dent upon the recuperation of the tissues and requires considerable 
time, three months to a year, to demonstrate a cure and the need of 
the patient is imperative. 



Fig. 543 



Fig. 544 





Same case as Fig. 544. Pus 
equalled cavity in volume. Right 
central has root end resorbed into a 
cup which held pus. Unfortunate 
canal filling. Left central chronic 
abscess with fistula. Right lateral 
seems involved but was vital. Posi- 
tion of teeth reversed in radiograph. 



Same case as Fig. 543. Centrals 
extracted. Bridge with open-faced 
crowns on laterals. Shows complete 
healing, though no curettement was 
done. Note bone septum in center. 



Hartzell 1 states that "An arthritis once started by tonsillitis or 
similar large foci can be kept going by an oral infection so slight as 
to be scarcely recognizable in the radiograph and systemic diseases 
are continued by surprisingly shallow gingivitis even when the larger 
local foci, doubtless the originators of the trouble are removed." 

Greeves, 2 in a late article, condemns all treatment of root canals 
having infections of the apex associated unless apicoectomy is a part 
of the program, claiming too great danger of continued apical infec- 
tion. He also condemns opening and attempting to refill cases show- 
ing partial root filling to the middle third when no granuloma is 
evident, claiming that a virulent reinfection arises. This may be due 
to his non-use of formocresol without an adequate substitute (see 
Arguments on page 495) . In severe systemic disease one or more apices 

1 Jour, of Nat. Dent. Assn., November 15, p. 339. 

2 Ibid., August, 1918, p. 789, 



BONE COMPLICATIONS 



563 



Fig. 545 



of roots may be saved for the purpose of making an autogenous vac- 
cine from the diseased tissue. This should be done and injected 
for a period at suitable intervals by a skilled laboratory physician. 

This is to raise the opsonic index against the bacteria in the joints, 
etc. While the writer has had no experience with the method it would 
seem that Wright's treatment with succinimide of mercury injections 
would be indicated in desperate cases not recovering by the former 
methods of treatment. It has been claimed that apical abscesses 
"dry up" with this treatment. If so, joints, etc., should be reached. 
(See Treatment of Pyorrhoea.) 

Granting that the root canal may be a proper avenue of treatment, 
the root canal is later mechanically opened, as shown on pages 448 
and 539, with care to penetrate the granuloma or abscess with 
broaches. The treatment of the granulomatous tissue consists in its 
sterilization, if possible, or stimulation to increased phagocytosis and 
granulation. This being diseased tissue there can be no harm in 
passing phenolsulphonic acid, 80 per cent., into the sac with this 
object in view. Nor can the writer believe 
that formocresol dressings in canals are in- 
jurious, provided antisepsis be attained. 
Ionization may be used (see page 496). In 
brief the treatment is as for pulp putrefac- 
tion (see page 493). 

. Bone Complications. — In any case of apical 
abscess necrosis or caries of bone may occur or 
the root end alone may become necrotic. A 
portion of necrotic bone may be sequestered 
and exfoliated or operative interference may 
be necessary. In carious bone the osteoporo- 
sis and ulceration may be progressive and in- 
volve much bone. Apicoectomy and the re- 
moval of any dead bone is the indication in 
simpler cases and extraction and bone re- 
moval in the more severe. The present demands of oral hygiene 
do not admit of partial measures. (See Apicoectomy.) The same 
is true if syphilis, scarlet fever, typhoid or mercury has caused the 
necrosis. The illustration (Fig. 546) shows a case of necrosis with 
two external sinuses along the lower border of the mandible associated 
with great pain or recumbency, rise and fall of temperature and 
occurrence of stupor and coma. The operation consisted of extrac- 
tion of the cuspid and first bicuspid, removal of the sequestrum, 
curettement of bone and drainage. 1 

1 Practice of Dr. Gilmer, description by Dr. Howard R. Raper, Dental Items of 
Interest, July, 1912. 




Blind abscess which 
developed acute symp- 
toms. Cured by extrac- 
tion of all three teeth. 



564 



CHRONIC SEPTIC APICAL PERICEMENTITIS 



Necrotic alveolar walls may result in advanced pyorrhea. It may 
also occur from the bruising of the periosteal lining of the alveolus as 
the result of extraction of a hypercementosed root, or from a bruise 
induced by forcible use of forceps in the removal of deeply seated 
roots. Possibly it may also occur from infection by apical 
abscess, etc., after extraction. 

Fig. 546 




The white line is artificial and shows the extent of the sequestrum (see text) . 
(Radiograph by Raper.) 



The clot seems to fail at times after extraction with anesthe- 
tics containing adrenalin or suprarenin. In some cases the socket 
may be free of blood for several minutes after extraction. Ragged 
gum margins may become gangrenous, although sometimes not. 
After extraction any loose margin of gum or rough edges of process 
should be trimmed up. 

The walls of the alveolus become infected by pyogenic organisms. 

The leaving of cotton tampons, placed as vehicles for pain-relieving 
agents, for an undue length of time also invites infection. 

The gum margins are perhaps sloughing; the bone may be 
exposed and exquisitely painful to touch, or it may be necrotic and 
insensitive superficially. The case is one termed "dry socket." 

Cases of general septicemic or pyemic infection from this source 
have been recorded. 



BOtfE COMPLICATIONS 565 

In the majority of cases the pain is of a deep, boring, continuous 
character. Reflex pains are also produced about the face. Much 
debility is caused by the wearing character of the pain, the loss of 
sleep and appetite, and probably also because of absorption of 
toxins. 

Treatment. — The mouth and, in so far as possible, the inflamed 
part must be sterilized. Probably mercuric chlorid in hydrogen 
dioxid (1 to 1000) will answer best. If the solution be used hot, 
whether it be mercurialized or not, the pain is much relieved. Talbot's 
iodoglycerol, one-fourth to full strength, is valuable and penetrating. 

Under mucous or conductive anesthesia all sloughing gum should 
be cut away, and acutely inflamed or necrotic bone should be 
cut away with large sterile burs until healthy tissue is reached. 
After washing out the debris and further sterilization a clot is to 
be induced by curetting if necessary. The mouth is to be kept 
sterilized and the patient is to be seen daily for a repetition of the 
curetting if the clot fail, or the alveolus may be gently packed with 
cotton saturated with balsam of Peru alone or with castor oil, equal 
parts, as a stimulant. Trichloracetic acid in saturated solution, or 
silver nitrate, or aromatic sulphuric acid may be used as a special 
stimulant and the balsam packing renewed. In ordinary cases one 
or two local treatments will be 

effective, but the tonic, antiseptic, FlG - 547 

systemic medication recommended 
under the heading of acute apical 
abscess is advised. 

An alternative proceeding may 
be adopted. A pellet of cotton wet 
with campho-phenique should be 
rolled in pow T dered orthoform and 
introduced into the socket after 

Sterilization with iodine, or a Stiff Showing the relations of an abscess 

j p , l p • upon a temporary tooth, with the crown 

mass made from Orthoform, Zinc f a developing permanent tooth under- 

oxid, and vaselin may be packed lying it. 
into the alveolus as an antiseptic 

and anesthetic. The repetition of this after five to eight hours will 
afford marked relief. (Jack. 1 ) Later the radical operation may be 
performed if granulation does not set in. While alveoli will fill with 
granulations in the absence of a clot filling them, such a clot seems 
to be the best protection against sepsis and a depressed scar tissue. 
In some of these cases portions of bone may exfoliate. In one obsti- 
nate case the capsule of bone surrounding the apex of the alveolus 
came away. 

international Dental Journal, 1905. 




566 



CHRONIC SEPTIC APICAL PERICEMENTITIS 



Chronic Septic Pericementitis in the Temporary Teeth.— Any of the 
chronic septic conditions described may occur upon the temporary 



Fig. 548 



Fig. 549 







' BmIU 




Dentin from the root of an abscessed 
tooth, showing the penetration of cocci to 
a depth of about T V mm. (-^ho m -); the 
side a to 6 bordered upon the canal. 
X 1000. (Miller.) 



teeth. The presence of resorption 
and of the permanent crown 
usually confines the inflammation 
to a point lower in the alveolar 
process than in the case of perma- 
nent teeth. The loose character of 
the structure causes the ulcera- 
tion to occupy a larger area, and 
the parts in chronic inflammation 
look more angry, but are fairly 
well tolerated. The treatment is 
practically the same for the curable 
cases; the others should be ex- 
tracted. The root canals when 
treated should be filled with absorb- 
able materials, such as paraffin or 
wax combined with aristol. Buckley 
recommends, as a canal filling in these cases, the use of a stiff 
mixture of calcium phosphate and formocresol (formalin, 1 part; 



:<> 



Sector of a cross-section from a dis- 
eased root: o, cementum; 6, stratum 
granulosum; c, very narrow and finely 
branched tubules; d, penetration of 
bacteria into tubules. X 150. 
(Miller.) 



CHRONIC APICAL ABSCESS 567 

cresol, 1 or 2 parts), to be packed into the pulp chamber and zinc 
phosphate quickly flowed over it; the cavity to be filled later. 

Johnson 1 suggests that a eucalyptol solution of gutta-percha (see p. 
479) be pumped into the canals and pressure exerted with temporary 
stopping until the solution appears at the fistula. The temporary 
stopping that does not interfere with filling integrity should be left. 

Septic Pericementitis at Bifurcations of Multi-rooted Teeth. — 
Teeth weakened by caries may fracture after filling in such a manner 
that the line of fracture exposes the pericementum at the bifurcation. 
The crack admits septic saliva, and a filling or fillings usually sink 
gingivally, wedging apart the two sections and admitting more 
or less food matter. If the canals of the sections have been pre- 
viously treated and filled, it is usual to find a more or less general 
pericementitis due to the wedging and septic irritation. It is an 
open question if such teeth can be saved so as to be hygienic and 
their extraction is advised, though occasionally one root may be 
utilized if it can be treated. 

Chronic Septic Apical Pericementitis (Non-purulent). — Continued 
apical inflammation of a low grade probably is a condition analogous 
to apical granuloma or the infection leading thereto. It may not 
show in a radiograph. 

Miller 2 has shown that root tubules are infected only for a short 
distance at their canal ends, so that infection from the perice- 
mentum via the cementum and dentinal tubules is highly improb- 
able (Fig. 548). The putrefaction produces gases, and these exuding 
slowly produce the irritation. If pyogenic organisms be present, apical 
abscess may at any time supervene, but, as shown in foregoing 
pages, subacute conditions may occur. 

Mayrhofer 3 has shown that even formocresol fails to sterilize all 
tubuli, so that bacteria, especially streptococci, grow back into the 
canal. Price and Brooks 4 demonstrated the great difficulty of steril- 
izing all parts of the root tubules with any germicide. If the canal 
filling be imperfect, and it is said that all are, it is obvious that apical 
infection may arise. These cases are puzzling. Can they initiate 
sufficient infection to cause systemic disease without a granuloma 
appearing in a radiograph? If so, then all canal filling stands con- 
demned as in the presence of such a possibility even apparent success 
may mean nothing but doubt and worry and the so-called "100 per 
cent, vitality" the only aim worth while. The only hope lies in the 
sufficient application of germicide of known germicidal power and 
tight root canal filling. Whether we shall really attain this end 
remains to be seen. 

1 Dental Cosmos, 1899. » Ibid., 1899. 

3 Items of Interest, March, 1910. * Journal of Nat. Dent. Assn., March, 1918. 



CHAPTER XVIII. 
NON-SEPTIC PERICEMENTITIS. 

Various grades of pericemental irritation, ranging from a mild 
arterial hyperemia to actual inflammation, may be produced by 
non-septic causes. 

The most satisfactory evidence that inflammation may be so 
caused is furnished by Talbot's experiments with the mercurialization 
of dogs. Beginning with healthy pericenienti, these were, after 
mercurialization of the animal, found to contain the round-celled 
infiltration characteristic of inflammation, and no bacteria could be 
found. Further evidence is given by the usual experimental study 
of inflammation with the mesentery of the frog. Simple irritation, 
even with antiseptic substances, produces the phenomena. Any of 
the causes which may produce inflammation may, if acting in more 
mild degree, produce arterial hyperemia. If the action of the cause 
be violent and then discontinued, as in the case of a blow, the inflam- 
mation resulting is acute, but may pass into a chronic form; but if 
the cause continue to act it produces a chronic inflammation. 

For purposes of description, non-septic pericementitis may be 
divided, according to its character, into traumatic and symptomatic, 
and, according to its location, into apical and general. 

TRAUMATIC PERICEMENTITIS. 

By traumatic pericementitis is meant a profound irritation of the 
pericementum, the result of mechanical violence applied externally 
to the tooth, or of instrumentation or chemical irritation of the 
pericementum through the root canal. 

Causes. — Violence Externally Applied. — Blows or falls deliver 
a force expended upon the pericementum and alveolar bone whether 
received upon the teeth or indirectly. Light blows produce peri- 
cementitis, heavy ones may cause fracture or partial or complete 
dislocation of teeth or fracture of alveolar bone. A severe degree of 
pericementitis becomes subordinate to the major accident. 

The biting of hard substances may fracture teeth (see page 225) and 
like biting of threads delivers a short sharp blow upon the peri- 
cementum. Overmalleting in building fillings is a similar cause. 
(568) 



TRAUMATIC PERICEMENTITIS 569 

Malocclusion, especially overocclusion, due to overfull fillings or crowns 

when occlusal, increases the length and throws the force of the jaw 
upon that tooth, when approxijmal it produces a similar effect by 
throwing cusps of teeth into malocclusion. The same effect is tem- 
porarily produced by wedges of rubber or wood, with least tape and 
traction cord and as a rule orthodontia usually has a similar effect 
if rapidly done. Malocclusion due to natural irregularity, so to speak, 
only exceptionally produces this condition, but malocclusion due to 
extractions and tipping may produce it usually in a mild form leading 
to slow degeneration of the pericementum (see page 587). When ex- 
tractions leave so few teeth that the others are overused non-septic 
pericementitis supervenes. Occlusion leading to this result has been 
called "traumatic occlusion." The looseness of a tooth from any 
loss of alveolar support as in resorption due to calculus or pyorrhea 
alveolaris means increased movement under ordinary forces of masti- 
cation and the mechanical production of non-septic pericementitis. 

The overstrain of a pericementum by clasping or the use of insuffi- 
cient piers for bridge work or its improper occlusion all produce 
non-septic pericementitis. These conditions will have further con- 
sideration. (See Overuse and Malocclusion, page 588.) 

The use of clamps or ligatures has produced gingivitis with which 
more or less pericementitis may occur. This injury may cause much, 
even permanent injury or mild injury only. 

Pathology of Traumatic Pericementitis. — There is inflammation with- 
out pus formation in the non-septic area. In more marked cases 
there is considerable bruise and consequent swelling causing extru- 
sion. Not infrequently the tooth is permanently elongated. Fre- 
quently a severe non-septic pericementitis is harder to cure than a 
septic one and degenerative changes may set in if chronic. If fracture 
occur and infection follows a true alveolar suppuration may occur. 
In some cases the blows cause pulp death and if sepsis enter apical 
abscess may follow upon the alveolar infection. 

Complicated by Sepsis. — Flaring or deeply placed gold bands, or any 
foreign body under the gum margin (see list of Causes of Gingivitis, 
page 603), may produce mechanical irritation so invariably accom- 
panied by septic complication that the production of a septic marginal 
pericementitis as well as gingivitis is inevitable. However, when 
removed the case rapidly cures so that the traumatic factor must be 
considered paramount, i. e., sepsis is implanted upon non-sepsis. 
Likewise any case of lateral chronic non-septic pericementitis may be 
complicated by sepsis at the gingival margin and eventually lead to 
pyorrhea (in the broad acceptation of the term). Also a pyorrhea 
pocket while causing a septic pericementitis at the point infected 



570 NON-SEPTIC PERICEMENTITIS 

must necessarily be accompanied by a zone of non-septic perice- 
mentitis higher up and to which resorption of bone or roots are 
referable. (Read page 588.) 

Symptoms and Diagnosis. — If the tooth is tender to touch or tapping 
the pericementitis is more or less severe according to the rebellion 
of the patient and force necessary to elicit the symptom. The gum 
may be swollen and red or not. If not and tapping is required to 
elicit response, the case is a mild one. The fact that the tooth may be 
vital and an external cause found as described puts the case in this 
class. Malocclusion is noted by means of carbon paper if slight by 
tooth movement or occlusion if profound. (See Malocclusion.) 

Prophylaxis. — All forms of external violence should, if possible, be 
avoided when deliverable by the operator, but accidental violence 
cannot be. However, as to biting nuts, thread, etc., patients should 
be warned. Malocclusion should be corrected. 

Prognosis. — Traumatic pericementitis in high degree in the young 
may be recovered from; but in the middle-aged and aged it may give 
rise to a series of degenerative changes which end only with the loss of 
the tooth. 

In cases due to looseness of the teeth, of course, septic primary 
causes have to be considered, but the pericementitis may be quite 
as much mechanically as septically produced. 

In all cases the extrusion caused by the inflammation adds another 
exciting cause of non septic pericementitis — i. e. , malocclusion, which 
aggravates the condition. 

Treatment. — The removal of the cause is paramount. In case of 
violence from a single cause as a blow, etc., only the effects can be 
treated. In mild cases of this type sedation of the gum is indicated 
by the application to the gum of cotton or gauze saturated with cold 
aqueous hamamelis or boric acid solution may be added (equal parts) 
to prevent sepsis in cases of possible fracture. Cold applications or 
bandages on the face or the ice-bag are always applicable. If fracture 
and suppuration have occurred this requires syringing of the part 
with antiseptic liquids and the above sedation. Derivation is always 
valuable in any such case (see page 527). Causes of malocclusion 
should be removed. In orthodontia milder force should be used. 

If the cause be some mechanical irritant at the gum margin, this 
should be removed and the case treated as described for gingivitis. 

The second principle of surgery is rest. This is required in all 
severe cases. 

As a preliminary measure the tooth is gently but firmly lashed 
to its neighbors by means of ligatures so that it is rigidly held. Splints 
may occasionally be necessary, but ordinarily varnish, zinc phos- 



TRAUMATIC PERICEMENTITIS 571 

phate or Kowarska's paste may be used to stiffen the ligature. (See 
Pyorrhea.) A swaged cap is to be fitted to a neighboring tooth to 
prevent occlusion. 

In cases involving several teeth, such as all of the incisors, two 
metallic plates are quickly swaged over metal models of the teeth 
to cover posterior teeth and raise the bite, and they are cemented 
in position to relieve the irritated teeth from occlusion. 

Violence Internally Applied. — If a wholly or partially vital 
pulp be torn from its apical connections, as in the use of pressure 
anesthesia, an apical traumatic pericementitis may be set up. This 
is usually transient. Secondary hemorrhage may occur and produce 
pericementitis. 

Excessive laceration of the apical tissue by means of barbed 
instruments, the inclusion of air or medicament under a root dress- 
ing or filling, the same exercising pressure upon the apical tissues; 
the same caused by biting on a temporary stopping, covering such a 
dressing; the mechanical irritation of a projecting root filling, pivot 
wire, broach, or drill, are all sufficient causes and should be borne in 
mind with intent to avoid but cannot always be avoided. 

The undue enlargement of the apex of the root canal or the passage 
of a reamer through the lateral aspect of a root may excite inflam- 
mation, and the perfect filling of the opening may be exceedingly 
difficult, so that if the tissues are not infected at the time, sepsis 
may later follow. Asepsis is in order. 

Cases due to perforation of the root and wounding of the peri- 
cementum, after the acute symptoms have passed, commonly assume 
an irritative and chronic type, the soft tissues included in the per- 
foration being in a state of chronic inflammation. Many of these 
cases become infected owing to the difficulty of completely sterilizing 
the apical portion of the canal which lies beyond them. 

The pericementitis produced by pressure of included air, liquid, 
or plastic root filling upon the apical tissue is often severe. Upon 
removal of the root dressing or filling the engorgement is relieved 
by the gushing of blood through the root canal. The inflammation 
may, however, continue unless sedatives be applied to the apical 
tissue via the canal. 

Chemical Irritation. — Externally caustics applied at the gum 
margins may produce a gingivitis with which pericementitis may be 
involved. The application of arsenic to a perforation may excite in- 
flammation and necrosis, which endangers the jaw. (See page 443.) 
The use of arsenic as a pulp devitalizer may cause a hyperemia of the 
apical tissue, following the hyperemia of the pulp, and causing slight 
tooth extrusion, which is aggravated by the malocclusion. As stated, 



572 NON-SEPTIC PERICEMENTITIS 

pulp hyperemias of any sort may act thus (sec page 403). This is 
not dangerous. (See page 435.) 

The undue use of escharotics, such as carbolic acid, sodium dioxid. 
sodium and potassium alloy, zinc chlorid, sulphuric acid, or mer- 
curic chlorid, in a pulp canal may excite an undesirable irritation. 
The limited irritation following their limited use is often more than 
offset by the advantages of the asepsis produced. 

One may view such an irritation with equanimity if asepsis and 
later comfort be attained in tissue already diseased as in apical granu- 
lomata or abscess, while in normal tissue, as after pressure anesthesia, 
irritation should be avoided. 

Diagnosis. — The fact of pericementitis is obtained together with 
the degree of severity as in other traumatic cases, but the root canal 
has a described or known history, or radiography establishes the facts 
as related under the causes. 

While in fresh cases the diagnosis is fairly easy owing to known facts 
in all cases only the absence of pus or a similar effect indicates non- 
sepsis and in any case infection may really be present unknown to the 
operator unless a laboratory test be made. In case of doubt, it is 
better to assume sepsis rather than make the test. 

Treatment. — When the apical tissues have been irritated by way of 
the canal, after the cause has been removed and the tooth canal made 
operable, sedatives, such as tincture of aconite or menthol in chloro- 
form, phenol-camphor, eugenol, or menthol-phenol (menthol, 3 parts; 
carbolic acid, 1 part; melted together) should be applied on cotton to 
the apical tissue by way of the root canal. Novocain may be added 
to any sedative oil. All cases of traumatic pericementitis of this type 
require the persistent use of counter-irritants, applied every other day 
to the overlying gum. (See page 391.) In cases in which the gum 
over the tooth is already inflamed this is not to be applied over the 
tooth but dental tincture of iodin is "spotted" around the area. 

Systemic derivation is also useful in the acute cases. In even 
mild cases the guarding of the extruded tooth against malocclusion 
is of advantage. (See page 527.) 

SYMPTOMATIC NON-SEPTIC PERICEMENTITIS. 

By symptomatic non-septic pericementitis is meant an aseptic 
pericementitis occurring as the result of systemic conditions, or of 
the action of drugs taken internally. 

If mercury be administered to patients in large doses for long 
periods, or in one or more massive doses, or if the patient have an 
idiosyncrasy to the action of this agent, or be a worker in mercurials, 



SYMPTOMATIC NON-SEPTIC PERICEMENTITIS 573 

an irritation of the salivary glands is excited, followed by looseness 
and soreness of the teeth and swelling of the gums; that is, a general 
pericementitis and maxillary periostitis arise. The patient has a 
metallic coppery taste, coated tongue, and fetid breath; the gums 
are puffy and bleed easily. In advanced cases the tongue and 
cheeks are swollen. Talbot's experiments on dogs show conclu- 
sively that a true pericementitis may be induced owing to the 
chemotactic properties of the mercury alone. (See Interstitial 
Gingivitis.) Potassium iodid administered in this condition relieves 
the maxillary periostitis and pericementitis; but the same drug 
administered in health, or for conditions other than mercurial 
poisoning, also causes irritation of the pericementum. Pilocarpin 
has a similar effect, though in much less degree. All of these drugs 
are partially eliminated by the glandular appendages of the mouth, 
and during elimination apparently act as local irritants. Lead 
poisoning may have a similar action. A blue line appearing on the 
gums is symptomatic. It occurs in painters and workers in lead. 
Lead has been found in the calculus on the teeth and even in the 
tooth substance. 

Patients who have a gouty heredity, or who are the subjects of 
active gout, frequently exhibit a tenderness of the entire pericemen- 
tum of one or more or sometimes all of the teeth. This pericemental 
disturbance may be the precursor of an acute outbreak of gout in 
the metatarsophalangeal joint. 

Scurvy — a now rare systemic disease, due to prolonged absence of 
vegetable diet — is attended by rapid inflammatory degeneration of 
the pericementum of the teeth and of the alveolar tissues. The gums 
are swollen and the teeth if loosened may fall out. 

Syphilis is also attended by pericemental irritation. This, of 
course, is of septic origin. 

In auto-intoxication by intestinal toxins or by leukomains in 
diseases involving general malnutrition, the irritants are probably 
in part eliminated by the gums, which are in turn irritated. (See 
Interstitial Gingivitis and Pyorrhea Alveolaris for further discussion.) 

It has been shown by Loup that mercurial stomatitis may be 
cured by mercury used as an oral antiseptic; therefore, the logical 
conclusion is that oral organisms play a part in the production of 
the local effects of mercury as is probable in many cases of systemic 
disease having oral symptoms (see pages 618 and 620) probably 
the mercury produces a local predisposition. This is further confirmed 
by the fact that if the teeth are attended to and oral prophylaxis 
practised before the administration of mercury to syphilitica, they 
tolerate greater amounts of the drug before salivation or stomatitis. 



574 NON-SEPTIC PERICEMENTITIS 

Touching this point Hartzell and Henrici 1 fed cats with calomel, 
producing mercurial stomatitis with loosening of teeth and abscesses 
from which and from the cervical lymph nodes streptococci were 
isolated (thus showing the action of oral streptococci upon tissue 
with reduced resistance). 

Treatment. — The drug should be discontinued, the disease, if 
present, should be antagonized, being referred to a physician, and the 
local complications, if any, should be appropriately treated, antisepsis 
being always advisable. If the pericementitis, gingivitis, and stoma- 
titis be mercurial, the drug should be stopped and an antisialagogue 
used, such as atropin sulphate, yio £?• eacn f° ur to six hours, until 
relieved. 

Potassium chlorate as a mouth wash, or internally, is useful if the 
stomach is not irritable. 

I^ — Potassii chloratis gr. xlviij 

Tr. myrrhse f 3ss 

Elixir calisayse q. s. ad f Siij — M. 

Sig. — Teaspoonful every five hours, or use as a mouth wash. (Hare.) 

Results of Chronic Non-septic Pericementitis. — If at any point of 
the irritated pericementum a constructive grade of irritation be 
maintained, the cemental tissue becomes hypertrophied (Fig. 550). 

Fig. 550 







If a more severe grade of irritation — i. e., low-grade inflammation 
— be present for a long time, the cementum and even the dentin 
of the root may be resorbed. Both of these results may go on 
concurrently at different points, or resorption may be followed by 
deposition of cementum if the conditions change. Even when 
primary causes are septic and a septic inflammation ensues, beyond 
the area of active inflammation there always exist non-septic areas 
having cell activity competent to construct or destroy by resorption. 
(See Granuloma.) 

1 Jour. Nat. Dent. Assn., May, 1917, p. 496. 



HYPERCEMENTOSIS 



575 



HYPERCEMENTOSIS (DENTAL EXOSTOSIS, EXCEMENTOSIS, 
HYPERPLASIA OF THE CEMENTUM). 

Definition. — By hypercementosis is meant a secondary deposit, or 
an increase of volume of the cementum of a tooth beyond the normal 
limit. It may be circumscribed or diffuse. 

Causes. — A constructive degree of hyperemia or very mild inflam- 
mation is the proximate cause, which may be excited by numerous 
primary causes, such as a projecting root filling, a projecting edge of 
crown filling, deposist of salivary calculus, the overlapping of a cavity 
margin by the gum, malocclusion, non-occlusion, the biting of hard 
objects, such as nuts or thread, the overuse of certain teeth, the 
habitual tapping together of teeth, the habitual chewing of tooth- 
picks, the gradual pressure of gas from dead pulps. The pressure of a 
tooth root against another root during eruption is a sufficient cause. 
(See Fig. 74.) The overcrowding of teeth in an arch has also caused 
this condition, as has also the impaction of a tooth (Fig. 169) . Chronic 
alveolar abscess or pyorrhea alveolaris may cause it by inducing 
about itself at a distance an area of hyperemia. (Aseptic Zone.) It 
also seems at times to be induced after pulp devitalization from any 
cause. Hypercementosis is a possibility in any case of chronic peri- 
cemental irritation competent to maintain constructive cementoblast 
activity; it represents a degree of irritation rather than any one 
specific cause. It has been discussed by some writers under the 
heading of Constructive or Condensing Pericementitis, and is 
analogous to subperiosteal deposition of bone especially in the form 
of a true exostosis or to osteosclerosis. (See page 49.) 

Fig. 551 




Hypercementosis. Outline of antrum well shown. (Radiograph by Lodge.) 



Situation. — Hypercementosis may be diffused over almost an 
entire root or several roots, or be localized as a distinct nodule at 
some lateral aspect, or exist as a circumscribed enlargement about 



576 NON-SEPTIC PERICEMENTITIS 

the apex of a root, or at the neck of a root. It is always located 
where the cause (hyperemia) has been produced (Fig. 551). 

Flagg noted that 75 per cent, of cases of hypercementosis were 
found upon posterior teeth, and that the teeth were usually of the 
character termed dense — i. e., the tissues of the individual were of 
recuperative type, tending to produce constructive changes. 

Pathology and Morbid Anatomy. — For some time after eruption 
the cementum consists of but few lamellae of deposit. It, however, 
reaches a maximum normal development at which it normally rests, 
as in the case of the physiological pulp cavity. As age progresses 
it is apt to be more thickly deposited at the expense of the peri- 
cementum, which becomes more attenuated. Whether this is due to 





Fig. 552 










h 




a^d 


, 


/ ■ / . 


■■';■... 


j'v;-" 


. Vy.'fVj 


- ■:'-' >? ' ; -': 


m 




. 




m 

■—Mi 1 ' 




Hypertrophy of the cementum on the side of a root of a lower molar near the neck 
of the tooth of a man: a, dentin; b, cementum; c, fibers of peridental membrane; 
from b to c the cementum is normal and the incremental lines fairly regular, but at 
d one of the lamella? is greatly thickened; at e this lamella is seen to be about equal 
in thickness with the others. The next two lamellae are thin over the greatest prom- 
inence, but one is much thickened at g, and both at h. These latter seem to partially 
fill the valleys which were occasioned by the first irregular growth. From a length- 
wise section. (Black.) 

irritants floating in the blood stream, or to the various local irritants 
above mentioned, to long continued use of the teeth, or to perfectly 
normal development, is not clear except for certain definite cases. 
Increased density of cementum may also be attributed to a similar 
pathology. 

Nodular and irregular forms arising from the general surface are 
clearly of abnormal type. 

Successive lamellae are deposited; the pericementum recedes, 
causing resorption of the alveolar process. Union of the bone and 
cementum (ankylosis) very rarely occurs. A resorption of cementum 
and dentin may occur at some point owing to a different degree of 
irritation, and in the area a new deposition of cementum may occur 



H YPERCEMENTOSIS 



577 



(Fig. 553, d). In some cases distinct areas of hypercementosis and 
root resorption are seen in close proximity. Chronic apical abscess 
may produce a denudation of the root end, and a short distance 
below at a point about at which the sac is attached and at which the 
zone of hyperemia would be present, an annular ridge of hyper- 
cementosis may occur. These are distinctly noted in granulomata (at 
times after extractions) . Areas of hypercementosis may be translucent 

Fig. 553 




Apex of root of an upper bicuspid tooth with irregularly developed cementum; 
a, a, dentin; b, b, pulp canals. The lamellae of cementum are marked 1, 2, 3, etc.; 
d, d, d, absorption areas that have been refilled with cementum. It will be seen that 
the apices of the roots were originally separate, but became fused with the deposit 
of the second lamella of cementum, and that in this regular growth began and was 
most pronounced. It has continued through the subsequent lamellae but in less degree. 
It will also be noticed that the absorption areas, d, d, d, have proceeded from certain 
lamellae. That between the roots has broken through the first lamella and pene- 
trated the dentin, and has been filled with the deposit of a second lamella. Other 
of the absorptions have proceeded from lamella which can be readily made out. The 
small points, e, seem to have been filled with the deposit of the last layer of cementum, 
while others have one, two, or more layers covering them. (Black.) 



or decidedly opaque, and sometimes the two are combined, a mottled 
appearance being produced, which corresponds to the constructions by 
the pulp in cases of secondary dentin and pulp nodule (see page 365). 
If the growth proximate another root, the pericementum may 
resorb at the point of contact and a deposition of cementum occur 
which firmly unites the roots in a union called concrescence. (See 
160.) 
37 



Fig. 



578 NON-SEPTIC PERICEMENTITIS 

It has occurred that a root filling protruding through a perforation 
has caused a diffused exostosis of the alveolar process. 1 The hyper- 
trophied process may be ivory-like in hardness. 

Symptoms and Diagnosis. — Many cases exist without active local 
symptoms. In no case is the color of the gum altered unless other 
disease than hyperemia be acting as a cause. In some cases there 
are symptoms of hyperemia expressed as a disposition to bite hard 
upon the particular tooth, or to grind upon it. A paroxysm of gnaw- 
ing pain lasting for some hours, and recurring at intervals, is also 
somewhat characteristic. Sympathetic hyperemia of the pulp with 
increased response to thermal changes may occur. (See page 388.) 
The gum may have slightly receded. 

Neuralgia, functional blindness, functional deafness, chorea, 
epileptiform fits, paralysis, cardiac neuralgia, insanity, and other 
related conditions have been cured by the extraction of hyper- 
cementosed teeth. 2 Milder symptoms of like character may of course 
occur. 

The treatment of teeth presenting obstinate symptoms of peri- 
cementitis, apparently due to putrefaction of the pulp, may at times 
be complicated by unsuspected hypercementosis and closure of the 
apical foramen may possibly be due to formations by the enclosed 
tissue. 

In such cases, if pulp or pericemental complication cannot be 
determined, suspicion should point to Ir^percementosis and an z-ray 
examination be made, by which means the condition may be posi- 
tively determined. As entire dentures have been extracted, tooth 
by tooth, in a vain endeavor to cure a neuralgia about the head, 
this means of diagnosis should not be overlooked. 

Treatment. — The treatment for hypercementosis may first be a 
conservative one if only slight annoyance be produced by it. 

Removal of a cause if found and counterirritation may be employed. 
The symptoms may disappear. If they do not, or they are severe 
when the patient applies, the tooth should be completely extracted. 
The operation of apicoectomy may be safely tried for apical hyper- 
cementosis. The bulbous condition of the root end may cause 
extraction to be difficult, and fracture of the root end may occur 
(or the alveolar wall may fracture). Flagg recommended that in 
such a case a fissure drill be passed about the circumference of the 
root end to remove the bony obstruction to its passage out of the 
alveolus, after which it may be lifted away with tweezers. In another 
method the root may be perforated by a drill and then divided into 

1 Garretson's Oral Clinic, 1884. 

2 Brubaker. American System of Dentistry. 



ANKYLOSIS 579 

two sections by means of a dentate fissure bur, after which the halves 
may be pushed together with a small elevator. If not then removable 
the fissure bur can now easily enlarge the alveolar constriction. In a 
third method an opening through the alveolar wall similar to that 
for apicoectomy may be employed. Local anesthesia is indicated. 
The use of alveolar forceps for the condition is little short of brutal, 
and only warranted by the impracticability of other means. 

Fig. 554 




Nodular hypercementosis on distal at first curve caused fracture. Removed by drilling 

alveolar process. 

Extraction for hypercementosis may cause considerable bruising 
of the walls of the alveolus, followed by inflammation accompanied by 
excruciating pain lasting often for days. The alveolus may refuse to 
granulate, and a septic condition result. The pain may at times be 
relieved by the injection of a 2 per cent, solution of novocain into the 
gum on both sides of the alveolus. After the surfaces of the alveolar 
walls have been sterilized as well as possible they are then burred 
away until tissue capable of granulation is reached. 

The alveolus should then be irrigated and a clot invited by causing 
a slight hemorrhage. The case is continued as for a dry socket" if the 
clot break down. (See page 564.) 

ANKYLOSIS (SYNOSTOSIS). 

By this is meant the union of bone and cementum, a condition 
analogous to ankylosis of bone. 

Hopewell-Smith 1 has described 5 cases, of which he offers the 
following explanation: (1) inflammation occurs and the membrane 
is changed into granulation tissue; (2) the cellular elements destroy 
portions of the bone and excavate the cementum; (3) the mass of 
granulation tissue is then ossified, joining the bone and cementum 
in a firm union. 

1 Histology and Pathohistology of the Teeth. 



580 



NON-SEPTIC PERICEMENTITIS 



E. C. Hice 1 has reported a case of a lady for whom an implantation 
of an upper bicuspid was done. In an effort made later to remove 
the tooth all attempts to loosen it in any degree with forceps failed. 



Fig. 555 





a b 

Resorption of roots, with immobility (see text). 

Fig. 556 



R 



c<- 



B 



Vertical section of a human tooth ankylosed to the jaw: R, root; B, bone of jaw. 
The absolute continuity of the two hard tissues is strikingly shown. From the col- 
lection of the late Storer Bennett. 3 (Hopewell-Smith.) 



In my own practice an implanted tooth was firmly immovable 
in any degree, though ten years in place: 2 The union may not be 
a true ankylosis in these cases, though doubtless bone has entered 

1 Private communication. 

2 This tooth has later fractured and the root was removed by division with a root 
reamer and the halves collapsed with an elevator. There seemed to be no resorption. 

:; Transactions of the Odontological Society of Great Britain. 



RESORPTION OF THE ROOTS OF PERMANENT TEETH 581 

areas of previous resorption. A remarkable case was shown the 
editor by Dr. J. Curry, of Philadelphia. Every pier tooth of 
four bridges was firmly ankylosed and immovable, yet large bays 
of resorption in each root necessitated extraction. This was not a 
plantation case. Fig. 555 a and b shows two of the teeth. 

RESORPTION OF THE ROOTS OF PERMANENT TEETH. 

By resorption of the roots of permanent teeth is meant the gradual 
removal of the cementum and dentin of permanent roots by phago- 
cytic cells existing in the adjacent soft tissue (osteoclasts). When 
occurring as the result of pressure by another tooth a tissue similar 
to an absorbent organ (Figs. 44, 45), as in resorption of deciduous 
teeth, is probably developed between them. 

Causes. — The proximate cause is probably in all cases a degree of 
irritation greater than that required to produce hypercementosis. 
Probably a mild non-septic inflammation exists or if septically pro- 
duced the tissue is capable of cell activity. Certain granulomas show 
macrophages present. (Thoma.) That an aseptic inflammation 
causes resorption or at least that infection is not necessary is 
shown by a specimen of Endelman's (Fig. 542.) in which inflamma- 
tory elements are shown outside the fibrous capsule of a granuloma 
which he has shown in several instances did not produce infection 
of media from outside while its contents did (see page 557). 
Talbot's demonstrations of interstitial gingivitis, a term meant to 
include interstitial pericementitis, show that it is a frequent cause of 
both root and alveolar resorption. (See Deeply Seated Gingivitis.) 
In other words, it is due mainly to an aseptic pericementitis at the 
point of resorption though the primary cause may be septic, i. e., 
resorption occurs in the zone of lesser inflammation inside of the zone 
of hyperemia and outside of the zone of stasis (see page 39) . 

The disease has been discussed by other writers as "Rarefying 
Pericementitis, " fairly analogous to osteoporosis. (See page 48.) 

Of primary causes chronic apical abscess seems to be a frequent 
one. Although theoretically the alkaline pus formed should neutral- 
ize acid formation, the fact of resorption remains, and is probably 
explainable upon the ground that it is produced by the granulation 
tissue formed about the root apex during periods of lessened pus 
formation or previously during a granulomatous period. 

Protruding root fillings or broaches are common causes (Fig. 557) . 
A peculiar resorption in the cervical third of two replanted incisors 
caused the fracture of one at the point of resorption and necessitated 
the removal of both teeth (Fig. 559) . Plantations are usually followed 



582 



NON-SEPTIC PERICEMENTITIS 



by peculiar resorptions over even the entire root. These are often 
filled in with bone causing a rigidity of the root attachment. Loose- 



Fig. 557 



Fig. 558 



Fig. 559 






Fig. 557. — Apical abscess and resorption, produced by a protruding broach. 

Fig. 558. — Deciduous cuspid crowned, mistaken for permanent cuspid which lay 
in jaw and caused resorption of root of permanent lateral. (Radiograph by Price.) 

Fig. 559. — Resorption at cervical third in two replanted teeth, one broken in 
consequence. Editor's practice. (Radiograph by Hagopian.) 



Fig. 560 



Fig. 561 





Case of extensive resorption about upper 
central. (Radiograph by Lodge.) 



Resorption of roots. (Radiograph 
by Lodge.) 



Fig. 562 



Fig. 5( 





Distal root of lower molar abscessed 
and resorbed, probably during granulo- 
matous period. 



Oveiused and loosened vital tooth. 
Root apex appears as though first re- 
sorbed then hyper cementosed. 



RESORPTION OF THE ROOTS OF PERMANENT TEETH 583 

ness of a tooth with the resultant excess of movement excites deeply 
seated gingivitis and resorption of bone and often of roots. Looseness 
of teeth from any cause may cause more non-septic pericementitis, 
looseness and resorption, though as a cause it seems to produce slight 
spicular resorption rather than large bays. Partial luxation as the 
result of a blow or fall produces the same result, the pericementum 
becoming thickened, the tooth loosened and extruded, and mal- 
occlusion, which is also a cause, being induced. 

A toothpick broken off in the gum tissue has produced resorption 
at the neck of the root. 

The descent of a supernumerary or impacted tooth upon a per- 
manent root has caused resorption, exposing the pulp of the resorbed 
root, and producing pulp reactions. This may be quite extensive 
before violent symptoms occur (Fig. 558). In one case both the 
buccal roots of an upper molar were removed by a supernumerary 
tooth, the crown of which fitted the resorbed root ends. 

Resorptions also occur in orthodontia, as when a cuspid is delayed 
and presses upon a lateral root. The resorption may be more distant 
than the pressure point. In orthodontia this may be explained 
by the extension of the phagocytic area or the induction of such an 
area about moving teeth; indeed, teeth cannot be moved without 
exciting a phagocytic action. 

Dewey, 1 following Hertzler, claims that rickets causing imperfect 
calcification of teeth is liable to be a factor in untoward resorptions 
in orthodontia, while tuberculosis neither interferes with tooth 
eruption nor calcification, but may interfere with proper physio- 
logical resorption because the phagocytes are elsewhere occupied and 
the absorbent organ is not fully developed. 

Calculus beneath the gum margin has produced resorption through 
the production of gingivitis. In one case noted four lower incisors 
presented the characteristic bays at a point one-eighth inch below 
the gum line. 

Some of the cases exhibit no tangible cause; the root resorbs 
apparently as the result of a peculiar reaction upon the part of the 
tissues of the individual, who may lose many teeth by this process — 
i. e. y a dyscrasia exists. The teeth may be non-carious and the pulps 
vital. In some of these cases neurasthenia or a uric acid diathesis 
seems to have some association with the condition (Fig. 565). 

Pathology and Morbid Anatomy. — Both resorption of cementum 
and its redeposition occur in deciduous teeth as physiological pro- 
cesses; at some aspect of the cementum the tissue becomes hollowed 

1 Items of Interest, May, 1914, p. 358. 



584 



NON-SEPTIC PERICEMENTITIS 



out, and later may be filled in by new cementum which is again 
resorbed. Resorption of tissue throughout the body is accomplished 
by means of multinucleated cells (macrophages, giant cells, osteo- 
clasts). At some part to be physiologically resorbed these cells make 
their appearance in contact with the tissue to be removed, and it 
gradually disappears, the layer of multinucleated cells constantly 
occupying the excavated territory known as Howship's lacuna? 
(Fig. 564). 

Fig. 564 









'tr fi ' *■ 




jy 'M*M 


'■ v , 




.^^n^k 


wfw 


W 4~-J^^H|Hh0^K^ 


] *flya"'- 




w -'ML 

■ 




Pfc- Ji :X * , . p' %. 


W- ■ -*MS flHSBHHHIIIHH 





Inflamed pericementum, osteoclasts in Howship's lacunae. (V. A. Latham.) 



If a foreign (aseptic) body be introduced into living tissues, it 
becomes surrounded by these cells, which in some cases effect its 
removal; in others, failing to remove the foreign body, connective 
tissue forms about it and encysts it; encystment may occur after 
partial removal by giant cells. 

The resorption of a root may be of any extent, from a slight spicular 
roughness of the apex of the root to almost complete removal of 
the root. 

Perforation of the root from side to side may occur, of course, 
involving the pulp canal, and, if the pulp be alive, obscure reactions 
upon its part may occur (Fig. 565). 

An area of marked resorption may occur at a point just beneath 
the gum margin and upon any aspect of the tooth. In this situation 



RESORPTION OF THE ROOTS OF PERMANENT TEETH 585 

it may simulate a cavity of decay beneath the gum. It occurs 
upon either vital or devitalized teeth, and may expose the pulp 
or the root-canal filling. The gum tissue is usually found within the 
cavity 'Flic test of a probable resorption is the grotto-like character 
of the cavity, the hard, rough inner surface and absence of decalcified 
dentin. Its surface differs from that either of a cavity of decay or an 
erosion. There is in cervical cases open to the mouth a possibility of 
mistake and that destruction of decalcified dentin by saprophytic 
bacteria has occurred as argued by Black from crown cavities con- 
taining fungous pulp tissue (see page 417), on the other hand even 
this condition may possibly be absorption. These cervical grottoes 
resemble the large one in Fig. 505, in which case no argument of 
caries applies. 

It is probable that in plantations the root acts as an aseptic foreign 
body; mild inflammation occurs, subsides, and giant multinucleated 
cells attack the tooth root and endeavor to remove it by solution; this 
they accomplish, in part, in spots; then a 
tolerance is established (mild inflammation FlG - 565 

becomes hyperemia) and connective tissue 
organizes about the roots; later, more com- 
plete regeneration is represented in the for- 
mation of bone; condition of a bony fixation 
is established, evidenced by the clear ring- 
ing note elicited upon tapping the planted 
tooth. 

ttt.,1 £ , ,• £ , i Idiopathic resorption 

With reference to resorption alter planta- Q f permanent root. The 

tions, Miller 1 records the following results of ba ^ u P° n tne side ex- 

his observations. The fixation of reimplanted forated G the P r^ot P6 as 

or transplanted teeth may be accomplished in shown. Crater-like re- 

,i sorption about apical 

three Ways: foramen. Pulp first de- 

1. By simple encapsulation of the root. vitalized on account of 

n "D ±1. u Jl i? x*x- i,'i persistent pain and the 

2. By the bundles ol connective tissue which tooth later extracted. 
fill up irregular absorption spaces, especially 

where the pericementum has not been present at that portion when 
the implantation was made (a pseudo-attachment). 

3. By direct union of the surrounding tissues with the living 
pericementum. He inclines to think this the only permanent 
attachment. 

He states that for the most part osteoclasts were few and that 
resorption was carried on by small round cells. According to Ribbert 2 
osteoclasts are not essential to resorption of bone. 

1 Independent Practitioner, 1887. 

2 Adami and McCrae: Text-book of Pathology. 



586 



NON-SEPTIC PERICEMENTITIS 



The inflammatory reaction and resorption is least when replanta- 
tion is practised, but may at times be pronounced in even those 
cases. If the socket of a tooth extracted for resorption be examined, 
a mass of soft tissue will be found occupying the locations corre- 
sponding to the areas of resorption (Fig. 566). No acid reaction can 
be detected with litmus paper, but, nevertheless, it is probable that 
the cells producing resorption excrete an acid capable of dissolving 
the tissue. 

There is some evidence of this in cases of enamel resorption occur- 
ring upon the crowns of impacted teeth which have never been in 
relation with the oral fluids, and about which there is no evidence of 
caries in the areas of dentin resorption also present. In the fortunate 
specimens of these cases a superficial decalcification of the enamel 
surface may be seen which can only occur as the result of acid action. 
(See page 214.) 



Fig. 566 




Resorption of distal root of a first 
molar. (Radiograph by Custer.) 




Diagram of a case of root resorption 
after secondary dentin had formed: SD, 
secondary dentin; AR, area undergoing 
resorption; peculiar central spire of sec- 
ondary dentin which has resisted the 
resorbent action. Specimen in possession 
of Dr. A. P. Fellows. 



Symptoms and Diagnosis. — The tooth may present symptoms 
of non-septic pericementitis, and may be loosened in advanced 
cases. In the early stages no looseness may be observed. In 
more advanced cases a strain suddenly applied causes a luxation; 
thereafter the tooth progressively loosens. 

The condition may be discovered by accident; evidences of mild 
pericementitis appear, and the pulp canal is opened to search for 
a cause. The pulp may be found alive; if alive, and it is killed, or 
if it is found dead, broaches pass suddenly into the mass of soft 
tissue underlying the root. The progressive loosening of the tooth, 
with its peculiar movement, is about the only constant symptom of 
the condition. 

In cases of live pulp this organ may be hyperemic or inflamed, so 
that increased response to heat or cold is felt and there may be the 
reflex pains of pulpitis, this, taken in connection with the tenderness 



DEGENERATION OF THE PERICEMENTUM 587 

upon percussion which can usually be elicited, and with the peculiar 
loosening of the tooth, is a diagnostic guide. 

Flagg 1 stated that reflex neuralgias occur in this condition, but 
that the most constant indication noted by him was a sense of dis- 
comfort about the jaws, vaguely associated with some one tooth. 
The patient is convinced that if the tooth were removed relief would 
follow. In the absence of the loosening, which may not occur until 
the root is nearly gone, the resorption is most commonly discovered 
by entering the pulp canal and finding its length much shortened. 
In some cases the resorption may be found near the gum margin and 
simulating a cavity of decay, from which it may readily be diag- 
nosed by its appearance when exposed by packing the gum away. 
Such cases appear to accompany a marginal gum resorption. (See 
page 584.) 

The x-rays should exhibit the condition with sufficient clearness 
to furnish an absolute diagnosis. In the case shown in Fig. 514, the 
cupped area does not show in the radiograph, though the side view 
exhibits it absolutely. 

Treatment. — If a diagnosis can be made, the tooth should be 
extracted except in the cases near the gum margin alone, which may 
be filled with plastic fillings. Even then the condition may progress. 

DEGENERATION OF THE PERICEMENTUM. 

It has been shown that long before there is any detachment of 
cementum and overlying tissues, such as denotes a true periodonto- 
clasia, the pericementum loses its histological characteristics which 
shows that degenerative changes have occurred, the normal fibers 
and cells being replaced by tissue, ill-defined in character, or in some 
cases the tissue takes on that characteristic ill-definition, so to speak, 
known as fibroid degeneration. Areas of degeneration among normal 
fibers, swollen or obliterated fibers, fatty degeneration, endarteritis, 
perivascular round-celled infiltration, general inflammatory infiltra- 
tion, fibroid appearance of the alveolar bone, hypercementosis and 
resorption of root and bone are noted in histological specimens and all 
are natural consequences of non-septic inflammation. As degeneration 
of any kind is a retrograde step toward death, naturally the vitality 
of such tissue is impaired probably through disturbances of its vas- 
cular system. Therefore, any inflammatory changes due to produc- 
tion of non-septic pericementitis by any cause, leads to its degenera- 
tion and predisposes the tissue to invasion by liquefying bacteria at 

1 Lecture on Dental Therapeutics. 



588 NON-SEPTIC PERICEMENTITIS 

the gum margin. The pericementum has occasionally been described 
as "torn away," "melted down," etc., but the probable explanation 
is as given above. Though almost evident this is difficult of verifica- 
tion, except by the analogy of the progressive destruction of the peri- 
cementum in pyorrhea alveolaris (see page 569). The above descrip- 
tion will fit the phenomena of the various phases of tooth loosening 
and loss. Thus, for example, in a case beginning with malocclusion we 
may have the following steps: (1) malocclusion; (2) non-septic peri- 
cementitis; (3) pericemental degeneration; (4) bone inflammation, 
degeneration, resorption; (5) consequent looseness of tooth from lack 
of support; (6) extrusion, increased malocclusion and further degen- 
eration from the higher inflammation due to increased irritation; 
(7) infection at gum margin inducing a purulent or non-purulent 
periodontoclasia. Beginning in the counter direction we have, for 
example, (1) calculus formation at gum margin; (2) marginal inflam- 
mation and infection; (3) purulent or non-purulent marginal peri- 
odontoclasia (pyorrhea alveolaris); (3) aggravation and penetration 
into deeper pericementum and gum tissues; (4) associated non-septic 
inflammation still deeper; (5) resorption of alveolar bone; (6) conse- 
quent looseness of tooth and further deep degenerations; (7) looseness 
as a cause of further inflammation with production of extrusion 
and malocclusion and thus worse effects of infection which either 
must be combated or the tooth, lost. 

It is for this reason that malocclusion may be either a cause, or 
result, of pyorrhea alveolaris. 

The causes leading to non-septic pericementitis may any of them 
produce pericemental degeneration if long continued. Those acute 
conditions just previously described are more apt to demand a prompt 
cure usually given while more chronic causes, such as overuse, abuse, 
non-use and malocclusion of teeth are the usual forerunners of the 
profound pericemental degenerations which ordinarily are not com- 
plained of until profound. In view of applied therapeutics they 
should be considered separately. 

OVERUSE OF TEETH. 

By overuse of a tooth is meant such a variety of occlusion that the 
tooth receives a greater stress than its neighbors, or than it is designed 
to bear, or the subjection of the tooth to unusual work. The stress 
may be received in the normal direction, but be excessive in amount. 
The most prominent cause of this condition is the loss of one or more 
other teeth, permitting undue stress to fall upon the neighboring 
teeth, or, in some cases, on far-distant teeth. The tipping of extracted 



OVERUSE OF TEETH 



589 



teeth puts them in malocclusion. Too prominent artificial crowns, 
particularly those of the all-gold type, cause a general increase of 
stress upon the pericementum. Enormously overfull contour fillings 
may establish a similar condition. Lack of firm approximal contact 
lessens mesial and distal support and ordinary use becomes over- 
working. When but few isolated teeth remain in one denture and 
have antagonists, the teeth are certain to be overworked. Isolated 
and other teeth to which are attached clasps of artificial dentures or 
too large pieces of bridge-work, are in the majority of cases being 
constantlv overstrained. 



Fig. 568 



Fig. 569 





Periodontoclisis due to overwork. 



Apical bone resorption due to overuse 
and looseness without discoverable peri- 
dontoclasia. 



There is a disposition to regard teeth as incapable of holding fixed 
bridge-work or at least of being normal in a fixed position when at 
work as is the case either with fixed or the usual type of removable 
bridge. As opposed to this the retention of normal individual move- 
ment of teeth by construction of removable bridges designed to per- 
mit it, is advocated. While the latter has yet to be demonstrated 
over a long period of years, it may be stated that the former when 
constructed upon sufficiently strong piers to begin with and hygienic 
conditions maintained has prevented far more looseness than caused it 
and been satisfactory for many years. Even in pyorrhea of moderate 
extent it "splints" teeth so as to prevent that mobility so destructive 
of bony support, on the other hand bridge-work has been placed upon 
teeth utterly unsuited to the stress or upon improperly treated roots, 
with disastrous results explainable by the description of pericemental 
degeneration above given or resulting apical infecaon. These cases 
merely illustrate bad judgment rather than the faults of fixed bridge- 
work as to pericemental strain whatever other faults it may have. 

Pathology. — Like any other functional part which is overworked, 
the pericementum is first stimulated, causing the vessels to dilate. 
Soon evidences of overwork appear, and the condition passes into 



590 NON-SEPTIC PERICEMENTITIS 

one of interstitial pericementitis; the tooth projects, and is loosened; 
the overlying gum deepens in color, and evidences of venous engorge- 
ment are common (interstitial gingivitis). The result of the con- 
dition is a softening and degeneration of the substance of the peri- 
cementum; the alveolar wall is involved in the degeneration, and it 
is resorbed to a greater or less extent. Cases have been seen 
at this point with the gum margins as perfect as in any normal 
tooth though a symmetrical resorption of margins may be present. 
In one marked case in which incisors met with a slight lingual 

Fig. 570 




Illustrating use of overarch bar. See text. (Gorman. 1 ) 

occlusion upon the lowers, forcing them labially, the teeth were 
as loose as in the average pyorrhea case, but the gum margins 
showed absolutely no pocket. At any stage of the disturbance 
marginal infection may occur, and the degeneration and destruc- 
tion of the pericementum be hastened by suppuration or other 
secondary degenerations establishing pyorrhea alveolaris. 
The symptoms, diagnosis, and clinical history are given in the 

Items of Interest, October, 1913. 



OVERUSE OF TEETH 



591 



above descriptions. The prognosis is the inevitable loss of the tooth 
if the causes be not removed, in which event the prognosis is governed 
by the extent to which the degeneration has proceeded. (See 
Interstitial Gingivitis.) These cases are often seen at a time when 
it is difficult to say which came first, the pyorrhea or the overwork, 
but the conditions of evident overstrain, noted over a period of years 
in the same patient without actual gum pockets, as when posterior 
occlusion is largely lost, and the usually prompt response to surgical 
rest lead to inference that overwork started the predisposition to 
pyorrhea in the actual pocket cases. Nevertheless in pyorrhea when 
the marginal inflammation has caused bone resorption to the point 
of tooth loosening the mechanical strain of occlusion is a cause of 
further overstrain and looseness. 

Fig. 571 




A case of pyorrhea alveolaris and overwork. Five natural and one artificial tooth 
mutually supported by holding against plate brace. Note restraint of right cuspid 
and central by clasp, artificial tooth bevels and T button and restraint of left teeth 
by clasp and button. This principle may be employed in ordinary plate work. Adap- 
tation made by burnishing thin pure metal to teeth model, and stiffening with solder. 
This work lasted seven years during which the patient was not seen. Upon return one 
tooth was found to have been out for some time and the general condition of the 
mouth required several extractions, a plate was substituted. Had the patient been 
regular, I believe this could have been extended a long time. 



Treatment. — The teeth, if in overocclusion, should be dressed off until 
properly occluded. Prosthetic appliances should not be so attached 
by clasps as to unduly move the clasp teeth, especially buccolingually. 
The U-clasps or movable clasps are worthy of consideration in this 
regard. The appliance should support the teeth laterally, if possible, 



592 NON-SEPTIC PERICEMENTITIS 

and occasionally the enclosure of the teeth by the plate clasps, with the 
hooks facing each other or a buccal embracing wire stay, is required, 
as, for example, where four lower bicuspids only are retained for 
support to the plate, yet where they also require support (Fig. 589). 
Where incisors are loose yet teeth must be inserted on plates, the 
judicious shaping of the natural and artificial teeth so as to afford a 
restraint of the natural ones against the plate festoon is useful (Fig. 
571). In some cases the festoon of a plate causes gingivitis and tends 
to cause loosening. This may be due to an improper looseness of the 
clasps permitting a rise and fall of the plate, or the inner edge of the 
festoon requires trimming. (A lower bar plate in which no contact 
except at clasp teeth is allowed because the bar lies beneath the tongue 
level and, of course, away from the teeth is an example of the principle 
involved in avoiding this class of injury.) No attempt is made, how- 
ever, to cause the artificial teeth to strike before the natural teeth, in 
the hope of giving surgical rest to these organs. Such attempts 
always result in failure, as they cause injuries to the tissues upon 
which the plate and teeth rest, which are more severe than the 
pericemental disturbance. Another fault in partial plate work is the 
embedding of the plate in the soft tissues so as to cause the artificial 
teeth to be drawn or pushed away from occlusion. Resetting the 
teeth on the same base if possible is a remedy and allowing slightly 
for the contingency is a fair precaution against it. If it occur, it 
defeats the object of the plate which is to take strain from natural 
teeth by dividing the work. Occasionally the type of clasp known in 
general as the Bonwill or Steadman having an occlusal lug, is used to 
prevent "sinkage." 

Properly adjusted bridge-work frequently does good service in 
these cases, provided the overoccluding tooth or teeth be first dressed 
down short of occlusion and are given a period of rest until the 
pericementum recovers. The bridge, if carefully planned, may be 
made to direct and control the stress received by the injured teeth. 
Joining the various bridges is useful. In this connection what is 
termed the "overarch bar" is a valuable device. The wire crossing 
the palate or passing around teeth from one bridge to another on the 
opposite side automatically throws some of the stress received by the 
diseased teeth upon teeth upon the other side of the arch, which 
naturally are forced in an opposite direction during mastication or 
at least lend their support. Fig. 570 illustrates this. 

The use of the Gilmore attachment is useful, the wire supporting 
the plate connects several teeth roots and gives them mutual support 
as well as attaches the plate. Some of these devices permit "rocking" 
unless care is used to have the gum tissues compressed by the plate 



MALOCCLUSION OF THE TEETH ■ 593 

before the "sinkage" is limited by the device. This rocking means a 
deadly stress upon the teeth to which it is attached. 

Improperly occluding artificial crowns should have this fault cor- 
rected by removing the excess of material or by setting properly 
made crowns. All crowns should have full mesial and distal contact, 
as spaces permit a wedging of teeth and injury of the interdental 
gum septum, as well as allow movement to occur. 

Overfull fillings should be reduced to correct proportions and 
shape and those lacking contour be built out. The use of the small 
overlapping pin described on page 611 is useful in conjunction at 
times. 

Surgical rest is the only hope of saving the tooth. 

MALOCCLUSION OF THE TEETH. 

Each tooth of a denture is not only designed to receive a definite 
amount of force, but to receive it in a particular direction Or direc- 
tions; any excess of this force, or alteration of its direction, is followed 
by abnormal stimulation of the pericementum and by its overstrain- 
ing. The effects following a general increase of stress have been 
considered under the previous heading. By malocclusion is here 
meant the constant reception of stress by the pericementum in 
directions to which it is quite unaccustomed, or which are not in 
accordance with the anatomical design of the tooth. It is a peculiar 
form of overuse. 

Causes. — Original malpositions of the teeth may cause their faulty 
occlusion usually less troublesome as such than as sources of uncleanli- 
ness and gingivitis, etc. The most prolific source of the condition is, 
however, altered occlusion due to those changes of position of the 
teeth which follow upon the loss of adjoining teeth. 

Artificial crowns, which do not occlude in correspondence with 
the other teeth are a common cause. Overfull fillings or those lacking 
in contour are another cause. 

The shifting of positions of the teeth, in consequence of patho- 
logical changes occurring in or about the pericementum, causes the 
crowns of teeth to occlude improperly. 

Pathology. — The conditions established are those of overuse in a 
milder and more insidious manner. A typical example of this condi- 
tion is that of a lower second molar which has gradually tilted forward 
in consequence of the loss of the first molar; or a central incisor which 
has altered its position in consequence of inflammation in or about 
the pericementum. Some portion of the tooth, an edge, which before 
did not occlude with an antagonizing tooth, is brought into occlu- 
38 



594 NON-SEPTIC PERICEMENTITIS 

sion; if the occlusion be not unduly forcible, no immediate degenera- 
tive changes are evident. If the occlusion be excessive, the peri- 
cementum is not uniformly affected, but the greatest stress is brought 
to bear upon some lateral aspect of the structure. It responds 
in the degree of the overwork, and inflammation and degenerative 
changes occur, which, if the active causes be not removed, gradually 
spread to other portions of the pericementum, and the phenomena 
noted in connection with overuse occur, but are not so general in 
distribution. The tooth becomes more movable in one or more 
directions — i. e., is loosened; it may develop some degree of tender- 
ness upon percussion, and the gum color toward the affected side 
deepens, although it may remain normal in other parts. As in the 
previous cases, infection may — indeed, is likely to — occur. In 
some cases the pericementum may degenerate and be destroyed 
about one root of a multirooted tooth, and remain about the other. 
It is to be remembered that a less degree of irritation may produce 
hypercementosis. 

Pyorrhea alveolaris in any form is a localized suppurative peri- 
cemental inflammation, which causes inflammation of the peri- 
cementum in general. Swelling occurs and the tooth is pushed up 
into malocclusion. Other teeth are sometimes urged out of occlu- 
sion by these. Such teeth may sometimes be dressed off one thirty- 
second of an inch before the overocclusion is relieved. A direct 
result of the strain and compression brought to bear upon apical 
tissue is the production of non-septic pulpitis with reflex pain and 
response to heat and cold (see Fig. 355). 

Diagnosis and Treatment. — In all malposed teeth a careful examina- 
tion should be made of their mode of occlusion. If the tooth exhibit 
tenderness and looseness, malocclusion is almost a certainty; it only 
remains to determine its direction. Placing the finger on the teeth 
while the patient occludes the impact is noted in marked cases ; as in 
pyorrhea a distinct buckling may be felt. 

The spots of faulty occlusion may be determined by placing a 
strip of carbon paper (articulating paper) over the tips of the antag- 
onizing teeth and having the patient bite; the spots of contact should 
then be ground away until the tooth is slightly short of direct occlu- 
sion. Fresh strips of paper are used, and the jaws moved laterally, 
as in mastication, to note other points of contact; these should also 
be ground away and the surface polished. 

It suffices in some acute cases to place a rubber dam or metal cap 
guard upon a nearby tooth for a day or two to prevent occlusion 
upon the sore tooth, which regains its normal position in the alveolus 
as the inflammation subsides. The grinding and guarding may be 



DISUSE OF TEETH 595 

combined, judgment being required. With the loose teeth, fixation 
is the best principle. 

Prognosis. — If the condition be not corrected every time occasion 
requires, the degeneration progresses until the tooth is lost. 

If marginal infection has occurred, purulent or non-purulent 
marginal pericemental liquefaction (pyorrhea alveolaris) may have 
to be considered. 

DISUSE OF TEETH. 

Definition. — By disuse of teeth is meant a degree of usage less than 
the amount which the forms and structure of the teeth and contiguous 
parts fit them for. The disuse may be absolute or relative; teeth 
may not occlude at all, owing to the loss of antagonists or to extremely 
irregular positions. 

Partial Disuse. — Causes and Pathology. — If soft food be used 
instead of that requiring vigorous mastication, or if one tooth of a 
side be diseased so that that side of the mouth is unused in mastica- 
tion, or if one of the antagonists of a tooth be lost, the pericementi 
of the teeth involved do not receive their proper amount of exercise, 
and a degree of atony ensues. 

This partial disuse has a more distinct relation to the health of the 
gum margin, which does not receive a normal amount of friction 
from mastication, and if this be not offset, in part, by prophylaxis, 
marginal gingivitis ensues. As a rule partial disuse signifies a form 
of malocclusion and though the used portion may not be in over- 
occlusion there may result change in position of the teeth especially 
if an extraction space exists. 

Infection and the formation of calculus increase the irritation to a 
marginal gum inflammation, which is liable to run into a pyorrhea 
alveolaris. This is the real significance of disuse as a cause. 

Diagnosis and Prognosis. — A diagnosis of disuse (relative) is usually 
made out by inquiring as to the food habit of individuals. It is 
excessively common in civilized communities, particularly among 
the well-to-do. 

Treatment. — Patients should be instructed to use the teeth for 
chewing. Prophylaxis should be instituted and if the cure will be of 
advantage and not worse than the condition, the occlusion should 
be corrected. The considerations are then purely mechanical. In 
the making of fillings, crowns, etc., the possibility of inducing a partial 
disuse must be considered and avoided, though even here the avoid- 
ance of fracture is at times to have first consideration, especially if a 
major portion of the occlusal can be left in good occlusion. 



596 NON-SEPTIC PERICEMENTITIS 

Absolute Disuse. — Teeth which perform no work directly in masti- 
cation, or indirectly by serving as abutments for a bridge-piece, 
may be said to be in a condition of absolute disuse. 

Results. — A tooth or root whose pericementum receives no stimulus 
becomes relatively a foreign body to the organism and is finally lost 
through a series of pathological changes. (1) It is possible that the 
impact of blood-pressure raises the tooth an infinitesimal distance, 
and being without antagonism it does not • wholly recover its nor- 
mal position, the aggregate of these infinitesimal differentials being 
expressed in protrusions. (2) Possibly lack of accustomed pressure 
allows a slight hyperemia, consequent swelling and accompanying 
protrusion not compensated for by occlusal pressure. Devitalization 
of the pulp sometimes lessens this, but is not advisable. 

This is at times a fairly rapid process, and occurs often after the 
trimming of teeth for bridge-work so as to interfere with the planned 
occlusion, unless the bridge be rapidly made. If unopposed, it 
extends progressively, the neck being usually exposed, though some- 
times the alveolar process becomes developed and lies on a lower 
level as though it had followed the tooth down. (It is hypertrophied.) 
Usually the bifurcation of a molar becomes exposed, calculi form, and 
the extrusion becomes hastened by marginal gingivitis. The tooth 
may be firm even though half its root length be exposed, though often 
it becomes looser than normal. Sometimes it strikes other teeth with 
a glancing motion. If the teeth in Fig. 572 were closer this would 
occur, and such a process (malocclusion) hastens the loosening. The 
opposite gum may be injured by such a tooth. Another effect is the 
wedging of food between the teeth owing to a favoring entrance, the 
laterally unsupported tooth wedging away and then closing upon the 
food. This injures the gum septum. (See Gingivitis, Fig. 578). 

Finally the loosening or the annoyance compels the removal of 
the tooth. 

The danger of marginal infection is always great in these cases. 
Some degree of infection, no doubt, exists in all of them, which 
serves to explain the increased rapidity of the degenerations. 

Prognosis. — If teeth can be directly or indirectly brought into use, 
so that their pericementi receive exercise, the cases may recover, 
provided the teeth are not loose and not too little root implantation 
remains. If loose their pericementi are degenerated and swollen 
and any excess work causes their loss so they should not have been 
used for bridge work. 

Treatment. — The treatment consists in bringing the teeth into use, 
if the degeneration has not proceeded too far. In crowning for a 
bridge pier it is customary to shorten the crown to the general occlusal 



FIBROID DEGENERATION OF THE PERICEMENTUM 597 

level, though even if a little longer and not in direct occlusion the 
tooth is brought into a sort of mastication which is useful if it does 
not introduce an element of malocclusion, i. e., if the distal or repelling 
strain upon its mesial slope is compensated for by the mesial strain 
upon a pier or piers more mesial to it, or upon a pontic tooth, for 
example, upon the cuspid of Fig. 572, or pontic bicuspid occluding 
with the mesial slope of the lower first molar. In such a case as this 

Fig. 572 




Absolute disuse and elongation of an upper and a lower molar; partial disuse of 
bicuspid; small abscess cavity in the bone about a root. (Philadelphia Dental 
College Museum.) 

grinding both the upper and lower molar occlusally and the intro- 
duction of an upper bridge is indicated. Later, extraction is inevit- 
able. The operation, when determined upon, should not be delayed, 
for not only are bacterial growths invited about the loosened tooth, 
but the soft tissues are frequently increased in volume, and if extrac- 
tion be delayed until complete local atrophy of the alveolar walls 
has taken place, a soft and spongy mass remains, which interferes 
with the comfortable wearing of prosthetic appliances in the future. 

FIBROID DEGENERATION OF THE PERICEMENTUM. 

Fibroid degeneration of the pericementum is a senile atrophic 
change occurring in teeth, the pericementi of which have run a 
healthy life course, but finally have become subject to senile marantic 
constitutional changes of not clear nature. The condition thus first 
defined by Hopewell-Smith 1 is further described as found in that 

1 Dental Cosmos, 1904. 



Fig. 573 




Fibroid degeneration of the pericementum: C, cementum; A, alveolus; F, fibers 
with decrepit nuclei. Transverse section. (Hopewell-Smith.) 



A _ 




H 



M 



Fibroid degeneration of the pericementum: C, cementum; M, degenerated peri- 
cementum; A, alveolus; H, enlarged (osteoporous) Haversian canals. Transverse 
section. (Hopewell-Smith.) 
(598) 



ACCIDENTS TO TEETH 599 

class of teeth of the aged which have resorbed alveolar margins and 
exposed cementum, but not necessarily subject to pyorrhea alveo- 
laris, though traumatic pericementitis may be present. In some 
cases the teeth may be firm. 

Pathohistology. — The chief characteristics are an increase in size 
of the fibers of the pericementum, the loss of their nuclei, their 
generally structureless character, and their arrangement in promi- 
nent bundles about large spaces (areolae). (See Fig. 573.) 

The fibers are firmly implanted in both bone and cementum. The 
cementum does not become hyperplastic (hypercementosed), but 
the bone becomes osteoporous and the Haversian canals contain a 
shrunken fibroid tissue resembling that in the pericementum (Fig. 
574). 

The gum tissue in the vicinity also undergoes retrogressive changes 
in sympathy, becomes less vascular and more fibroid. 

The condition may persist without inflammatory or suppurative 
changes, though it may act as a cause of obscure neuralgia or as a 
predisposing cause to pyorrhea alveolaris. 

Hopewell-Smith points out that the areolar spaces may admit 
microorganisms to deep parts, thus predisposing to antral disease or, 
possibly, osteomyelitis. (See Marginal Atrophy of Gum.) 

Treatment. — There is no treatment possible beyond that for any 
associated condition or extraction if it be a cause of pain. 



ACCIDENTS TO TEETH. 

Apart from fracture of the teeth by accident, several interesting 
accidental conditions involving therapeutics require consideration. 

Teeth Driven into Alveolar Process. — Blows, falls, etc., have occa- 
sionally caused teeth to be driven forcibly into the jaw. The condi- 
tion may be complicated by fracture, in which case the judgment 
of the operator must be exercised. If the tooth be not fractured 
it may be drawn down with forceps and ligated in place until firm. 
The use of zinc phosphate upon the ligatures, if possible to use it, 
renders them more rigid. Splints may be used. If evidence of pulp 
death be noted by subsequent test, or apical pericemental inflam- 
mation, the pulp should be removed. 

Luxation or Partial Dislocation by Accident. — Teeth may be par- 
tially knocked out and driven either lingually or buccally. The pulp 
connections will be ruptured, as a rule, but after asepsis of the parts 
by means of antiseptic sprays the teeth may be pressed into place, 
and if ligated or splinted may again become firm by deposition of 



000 NON-SEPTIC PERICEMENTITIS 

bone about them. The pulps nearly always give evidence of death 
so that they should be later replaced by canal fillings. 

Mendel Joseph and Dassonville 1 record experiments on dogs 
showing a vital attachment of the pulp of an immediately replanted 
tooth. They used strictly aseptic precautions. 

Occasionally evidences of reattachment of pulp have been recorded 2 
even after total displacement. (See page 367.) If the accident result 
in elongation of the tooth with production of a chronically spongy 
pericementum, the operation of replantation should be performed. 

Total Dislocation of Teeth by Accident — If the accident or a mal- 
advertence in extracting another tooth result in total displacement 
from the mouth, the tooth or teeth may be prepared as for replanta- 
tion (see Plantation), and under aseptic precautions replanted in their 
alveoli. If held by ligatures or splints they will usually become firm. 
If the teeth are kept moist in a mild antiseptic a short delay if neces- 
sary does not prevent success, though clot and granulations must be 
swept out. The moisture also prevents the bleaching due to dryness 
which is usually fatal to good color. 

Attachment of Teeth. — Two or more teeth may be attached by the 
intervening alveolar process, fracture of which may cause both teeth 
to be removed in extraction. In a few cases of loose deciduous teeth 
the gum has been sufficient attachment to cause the removal of two 
teeth at once. 

In some cases the tough, fibrous nature of the pericementum 
causes the alveolar bone fractured by the leverage upon it to remain 
attached to the tooth, and Fig. 168 illustrates te'eth attached by 
union of pericementum only. 

Fracture of the Alveolar Process. — Slight fractures of the alveolar 
plate are of little consequence, as a rule. In some cases one plate 
may be fractured, and unless removed with the tooth, may usually 
be pressed back into place. Reunion may be looked for if reasonable 
asepsis be maintained. Fractures of the alveolar process from blows, 
kicks, etc., upon the jaw may become septic and sequestra may 
form, necessitating removal of both bone and teeth. Such fractures 
should have immediate attention. The writer once handled a delayed 
case in which about six plaques of alveolar bone about 1 x f inch each 
were bloodlessly removed with tweezers after loosened teeth were 
extracted. They came from both lingual and buccal sides of the man- 
dible. A kick by a horse caused this splintering comminution of 
alveolar process and body of mandible without actually fracturing the 
jaw transversely. The gums on both lingual and buccal sides were 

1 L'Odontologie. See Dental Cosmos, 1906, p. 1060. 

2 Kirk and W. Trueman. 



ACCIDENTS TO TEETH 601 

not especially affected nor was there much suppuration. Unfortu- 
nately I was leaving for a foreign country within a few days and had 
to refer the case to a hospital so have no record of the outcome. 
Fractures of the maxillae should, of course, be immediately reduced. 

Hemorrhage following Extraction. — Even in the absence of hem- 
ophilia postextraction hemorrhage may be somewhat severe, and 
is well controlled by a little tannic acid or powdered alum and thymol 
upon a pellet of cotton, or nosophen gauze wet with phenolsodique. 

If necessary a linen compress should be placed over it and a Barton 
or Garretson bandage applied. The internal use of calcium chlorid 
or other hemostatic is indicated if the bleeding be continued. (See 
page 30.) 

Lacerations. — The tongue, floor of the mouth, etc., may be lacer- 
ated by the careless use of forceps, and the lacerated parts should 
be irrigated with antiseptics and the mouth kept under astringent 
antiseptics while the parts are healing. Shredded gum margins 
should be trimmed up to prevent sloughing. 

Postextraction Aveolitis. — This has been already discussed. (See 
pages 564 and 569.) 

For ordinary transient pain, phenolcamphor with or without 
menthol added or equal parts of phenolsodique and laudanum are 
useful applied on cotton. Preparations of novocain, orthoform, etc. 
are also indicated. Hot salt water held in the mouth is analgesic, 
styptic and stimulant. 



SECTION VIII. 

PERICEMENTAL DISEASES BEGINNING AT 
THE GUM MARGIN. 



CHAPTER XIX. 
GINGIVITIS. 

The diseases which begin at the gum margin are all inflammatory, 
and are due to mechanical, chemical, and infective local irritants, 
and probably may be due to overexcitation of the gum tissues by 
leukomains or other toxic products which are formed intrinsically 
within the body in malnutritional processes, also to overexcitation 
by certain drugs, both of which the gum is endeavoring to eliminate. 
(See Symptomatic Non-Septic Pericementitis.) The inflammation 
resulting is termed gingivitis. Many mechanical or septic causes 
which produce pericementitis, such as overuse or apical abscess, 
finally induce an inflammation in the alveolar bone (osteitis), and 
later an inflammation of the gingival tissue. In reverse order, 
inflammations beginning in the gum, reach the bone, and later the 
pericementum. It is plain then that pericementitis and gingivitis 
are often associated, and at the gum margin are almost inseparable. 
(See Fig. 577.) 

If at any stage of a gingivitis as is of mechanical or chemical 
primary causation, infection enter the inflammation becomes septic, 
If non-pus-fcrming organisms as the streptococcus brevis (salivarius, 
viridans) a granulomatous infective, chronic inflammation may be 
produced and if pyogenic bacteria are later established, pus is formed 1 
(pyorrhea alveolaris of the pus variety). Some writers treat of all 
cases of gingivitis as cases of pyorrhea, advanced or incipient, and 
in view of the fact that a simple gingivitis may become a pyorrhea 
there is some justification from a preventive standpoint; as well as 
from the above bacteriological viewpoint; nevertheless, there* are 
so many phases of gingivitis that for purposes of discussion and 

1 Hartzell and Henrici: Journal National Dental Association, May, 1917, p. 492. 

(603) 



604 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

applied therapeutics it is advisable to specify the various forms that 
may exist. 

If confined to the gum margin it is properly designated marginal 
gingivitis; if the inflammatory elements (leukocytes and exudates) 
have infiltrated the deeper connective tissues it may be called deeply 
seated gingivitis or interstitial gingivitis. If a pus flow from the 
alveolus accompany the deeply seated gingivitis the condition of 
pyorrhea alveolaris is established. 

With any of these conditions an hypertrophy or an atrophy may 
be associated, which, on the one hand, may result in hypercementosis 
or exostosis or thickening of gum, or, on the other, in resorption of 
gum or bone. 

MARGINAL GINGIVITIS. 

Definition. — By marginal gingivitis is meant an inflammation con- 
fined to the margins of the gums about the necks of the teeth. 

Causes. — The causes of marginal gingivitis are local and general, 
which may be subdivided into predisposing and exciting. Both 
local and general causes may be in action at the same time. 

Local Causes. — The anatomy of the gum margin should be 
considered. 

Between the free gingival margin and the enamel exists a space 
considered normal (Fig. 577). As the soft tissue about the teeth can 
be distended by means of oxygen blown into this space 1 (see also page 
504) it is evident that intercellular spaces open into it. Considering 
in addition the presence of veins and "glands of Black" it is evident 
that infective material entering the gingival space may under mastica- 
tory pressure (which in the aggregate is estimated by Hartzell to 
average about a ton per day) be forced into the spaces or vessels 
to be carried into the pericemental tract, which at the gingival margin 
is in close conjunction with the gingiva (Fig. 577, Gg). 2 

Doubtless much phagocytosis occurs protecting the gingiva, but 
when this is inadequate inflammation may occur from bacterial 
plaques on the teeth which may generally be demonstrated with 
iodin disclosing solutions. There is further evidence in that prophy- 
laxis or plaque removal as a means of cure succeeds as a rule. Their 
presence means quantitatively, 20 to 600 millions of bacteria to the 
milligram (Kligler), and qualitatively streptococci, staphylococci, 
pneumococci, spirochetes, fusiform bacilli and protozoa (Hartzell, 
loc. cit.). 

1 Journal of National Dental Assn., 1916, p. 177. 

2 Also noted by Talbot in text-book Intestinal Gingivitis. 



MARGINAL GINGIVITIS 
Fig. 575 



605 




Diagram of glands of peridental membrane. (Black.) (Also called epitheli 
root sheath of Hertwig.) 

Fig. 576 




Cm, 



Glands of Black. Epithelial structures: Ec, epithelial cord, apparently showing 
lumen; C&,<cementoblasts; Cm, cementum; D, dentin. (See Fig. 134.) (Noyes.) 




Fig. 577 




Longitudinal section: Ep, epithelium lining the gingival space; Gg, gingival gland 
so-called; D, dentin; N, Nasmyth's membrane; Du, duct-like structure stretching 
away toward the gingivus from the epithelial cord, seen at Ec; Cm, cementum, 
separated from the dentin by decalcification. X 50 (about). The long space next 
to the tooth is made by the detachment of the soft and band tissues. The space 
between N and Ep is the gingival space. (Noyes.) 



MARGINAL GINGIVITIS 607 

Mechanical causes produce direct irritation; these are deposits of 
salivary calculus resting upon the gum or beneath the gum margin; 
fillings projecting beyond cavity margin; the edge of a bandless 
crown, the edges of a poorly fitted crown band and the putrefaction 
of food, etc., collected in the places from which cement has washed 
out; gum overlying cavity margins or edge of root to which a crown 
is not adapted or of a root with occlusal face under the gum ; bruising 
of the gum margin by food crowded between teeth and removed 
by toothpicks; the fermentation of such crowded food. 

The lack of contact or too light contact of approximal surfaces, 
whether due to faulty operations or induced by the wedging action 
of tooth-picks or floss silk, causing a general non-septic pericementitis 
and bone resorption (looseness of teeth) are contributory to the 
wedging of food. 

The mechanical action of toothpicks or floss silk improperly crowded 
upon the gum margin; projecting edges of artificial crowns or bits 
of cement used in their cementation; toothbrush bristles; fragments 
of toothpicks, bones, or oyster-shells, etc. ; rings of rubber or of torn 
rubber dam or ligatures left in position; rubber or tape wedges 
forced into the gum; the crowding back of a gum by ligation 
which produces ischemia for hours; improper contact of the edges 
of prosthetic plates its clasps or other appliances about the necks of 
teeth; injuries inflicted by rubber dam clamps, wedges, ligatures, etc.; 
the eruption of teeth through the gums, bits of fractured alveolar 
bone undergoing exfoliation. Pontic teeth may occasionally be 
embedded in gum which has grown up around them. It is probable 
that the movement of the porcelain against the gum combined with 
a possible sepsis induces a slow development of gum which further 
presses against the porcelain. Inflammation occurs. The vicious 
circle continues. 

An interesting case of recurrent epileptic attacks was proved due 
to a toothbrush bristle forced into the gum. 1 

The action of any of these causes may be complicated through 
the infection of the mechanically irritated part by oral bacteria. 
An excellent example occurred in the editor's practice. A perfect 
gum margin was irritated by the margins of a gutta-percha cap 
used as a remedy for hyperemia of the pulp. Pyogenic organisms 
produced a marginal suppuration which subsided upon removal of 
the cap. 

The pressure of plates into gum tissue either at their edges or when 
slight projections exist may even cause superficial ulceration. While 

i Dental Cosmos, 1910, p. 594. 



608 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

not marginal gingivitis it illustrates the combination of mechanical 
and infective causes. 

All forms of marginal gingivitis are to be considered as incipient 
inflammations which, let alone, may lead to deep-seated inflammation 
and tissue destructions collectively called pyorrhea alveolaris. Even 
if the causes of pyorrhea are infective (see pyorrhea) they act to first 
produce a marginal gingivitis. 

Excessive smoking and the use of alcoholic liquors produce local 
irritative effects, resulting in catarrhal stomatitis and gingivitis. 

Lack of exercise or brushing of the gums produces an atonic 
condition of the gum margin, predisposing to gingivitis of infective 
character. Too persistent brushing with stiff brushes may be 
equally injurious by causing marginal irritation. 

A variety of ulcerative marginal gingivitis exists which tends to 
rapidly penetrate the tissues and while it may cause pyorrhea, usually 
erodes the outer portion of the gum margin rather than destroys the 
pericementum as in pyorrhea. The gum margin has a pasty, slough- 
ing appearance, and the gum about several teeth may be involved. 
Vaughan 1 describes it as covered by a grayish necrotic covering which 
when rubbed off leaves a sensitive bleeding surface, the deposit being 
accumulated rapidly in an hour or two. He found the bacillus fusi- 
formis and spirillum which work in symbiosis in Vincent's angina. 
In the severe cases he describes fever, dysphagia, headache, malaise, 
nausea, marked salivation, loss of appetite, increased cardiac and 
respiratory action, and glandular enlargement as associate phenomena. 
It often extends to the tonsil and may extend to the lungs. 2 Fever 
of low grade is an accompaniment. (See Vincent's Angina.) The 
breath is offensive and characteristic. Hinman 3 gives the following 
bacteriological technic: "A smear is made with a platinum loop from 
ulcerating surface to a ground glass slide, carefully fixed over the 
flame of an alcohol lamp, stained with carbol-f uchsin for a few seconds, 
washed, stained with methylene blue for three to five minutes, washed 
and dried, examined for Vincent's spirochetes and fusiform bacilli 
which are unstained, being Gram-negative. They usually appear in 
large numbers." (See Fig. 580.) Syphilitic chancre may begin at the 
gum margin, and there is no reason why aphthae should not be so 
located though usually elsewhere. 

A form of phagedenic pericementitis causing very rapid destruc- 
tion of the pericementum and loss of the teeth without loss of alveolar 
wall has occasionally been noted. In one notable case two upper 

\ Dental Cosmos, 1912, p. 651. 

2 Hinman: Dental Cosmos, 1916, p. 1352. 

3 Dental Cosmos, December, 1914, p. 1354. 



MARGINAL GINGIVITIS 609 

incisors came away three weeks after an ulceration appeared about 
their gum margins. The patient wore the teeth for several weeks 
in situ, and could remove and reinsert them at will. The alveolar 
walls/were bare, but intact. There was but little pain. The alveoli 
healed after removal of the teeth and the freshening of the bone. 
There was no bacterial examination made at the time (1896). Occa- 
sionally the gum margin on a buccal side as a rule becomes invaded 
by bacteria and a granulomatous swelling occurs, sometimes this is 
the forerunner of a pyorrhea pocket and sometimes a distinct abscess 
occurs in the tissue of the gum (a gingival abscess). 

Cook has shown that stimulant and astringent washes, if used 
to excess, have a degenerative influence upon the gum margin. A 
too powerful formaldehyd wash has the same effect. 

The production of deeply seated gingivitis by causes of systemic 
or drug origin involves a marginal gingivitis, but marginal gingivitis 
is not always produced by local causes of interstitial gingivitis; at 
least, not at first (see page 588). 

Systemic Causes. — These are the same as for Deeply Seated Gingi- 
vitis, which (see page 616). 

Pathology. — The pathology of marginal gingivitis is that of an 
inflammation located in a peculiar situation — i. e., in the marginal 
gum tissue — and tending to spread into the deeper interstitial tissues. 
(See Pathology of Deeply Seated Gingivitis.) As shown above 
when pyogenic bacteria enter, a pus flow or pyorrhea, or in some cases 
a septal abscess or marginal abscess, supervenes. These conditions 
discussed above and on page 617. 

Symptoms. — The symptoms of marginal gingivitis depend upon the 
cause and degree of inflammatory action. When mechanical 
causes are acting the gum presents an inflamed appearance; it is 
swollen, of a bright red or purplish color, very sensitive to touch, 
and bleeds readily, growing around an irritating pontic tooth it may 
appear as though the latter had sunken into it. Likewise it may 
appear to have grown up between a plate festoon and a tooth, and at 
times apparently be merely hypertrophic rather than inflamed. 

If a calculus rest against the gum, the latter may present a raw, 
chronically inflamed surface in contact with it. A ragged, red, 
split margin of gum is often associated with calculus upon the labial 
surfaces of lower incisors, cuspids, and bicuspids, and upper cuspids 
and bicuspids. At times the lingual surfaces of the lower incisors 
present such an appearance. If subgingival calculus be present, 
the gum margin, if markedly affected, appears loosened, and is of 
a flabby appearance and purplish in color. In some cases the gum 
margin appears thickened or hypertrophied. 
39 



610 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

A bloodshot appearance — i. e., enlargement of terminal vessels — 
is often seen in gingivitis. 

In cases due to unhygienic conditions — i. e., food collections or 
vitiated secretions about the necks of teeth — a raw, red, outer 
surface of the gum margin is noted, particularly in young persons. 

In stomatitis ulcerosa a yellow, pasty ulceration of the gum mar- 
gins may occur. It is rodent in character, very painful, and may 
cause rapid loss of the pericementum and of the tooth. (See Vincent's 
Angina and page 608.) In gingivitis due .to oral infection by the 
coccus of gonorrhea an intense gingival inflammation with looseness 
of the teeth, pyorrhea alveolaris, and profuse salivation, may occur. 1 

Talbot 2 describes a greenish-gray glazed surface of ulcerated 
raw gum in two cases of profuse interstitial gingivitis due to the 
gonococcus. 

Stein is inclined to doubt the etiology. 3 

Bloodgood 4 describes a general ulitis in which the teeth may be 
almost buried as a concomitant of acute leukemia. 

The classification of the gingivitis depends upon the cause and 
progress of the disease. 

Prognosis. — If the case has run an acute course and is due to the 
action of mechanical causes plus infection, recovery is usually prompt 
upon the removal of the cause and sterilization of the injured part. 
In the chronic cases due to the more slowly acting mechanical and 
infective causes combined — e. g., salivary calculus plus infection 
— much deeply seated gingivitis may have occurred accompanied 
by pericemental and alveolar resorption. This usually constitutes 
a permanent loss. If the gum margin is in a state of atony or inflam- 
mation as the result of collections of bacteria, etc., upon the cervices 
of the teeth, their condition may be improved by frequent prophy- 
laxis. 

Treatment. — The treatment of the condition consists in removing 
the source of irritation and restoring the normal circulation in the 
parts. If the source of the disorder be in some underlying constitu- 
tional condition, the symptoms may be ameliorated, although not 
entirely cured, by the correction of the general disorder. 

Cases due to mechanical irritation are commonly confined to one 
or several teeth, rarely to an entire denture, except cases continued 
in consequence of deposits of scaly calculi beneath the gum margin 
or under plates. Foreign bodies, such as bristles and fragments of 

1 Vines. British Journal of Dental Sciences, 1903, and Dental Cosmos, 1903. 

2 Dental Cosmos, 1905. 

:; Bacteriology in its Relationship to the Oral and Nasal Cavities. Items of Interest, 
1914. 

4 .Journal of National Dental Association, 1915, p. 8. 



MARGINAL GINGIVITIS 



611 



bone, should be removed. Projecting fillings or overhanging crown 
margins should be made flush with the general tooth surface. Plates 
permitting gum to develop between the festoon and tooth should 
either have material added to a perfect fit or be filed ^away to 
remove the plate margin to a distance. Salivary calculi should be 
removed. When food crowds upon gum margins between teeth, 
lateral or mesiodistal contacts should be established either by con- 
touring filling, introducing a bridge which establishes such proximal 
contact, or in some cases by wedging at some convenient point so 
as to crowd several teeth together, then introducing a contour filling 
or inlay. The contact should exist just a little to the gingival of the 
marginal ridges and not be too broad and should be well rounded. 

Fig. 578 




Marginal gingivitis located in septal tissue between upper second and third molar 
(see text). Also shows anterior drifting of second molar, due to extraction of first 
molar early in life. 



In another phase of this condition in the writer's own mouth the 
extraction of a lower third molar allowed the distal cusp of the 
lower second molar to wedge between the upper second and third 
molars, so that the third molar was pushed distally and shredded 
food packed in simultaneously causing extreme and annoying gingi- 
vitis. In such a case if grinding the cusps of the antagonizing 
molars does not relieve, only extraction or firm attachment of the 
third and second molar will give relief (Fig. 578). In a few similar 
cases where fillings were present the fillings have been overcontoured 
and a clasp metal wire imbedded in a groove in one filling and the 
other pointed end allowed to rest in a slight groove in the adjoining 
filling. In this it plays freely but prevents the crowding of food, 
though food may float in laterally without direct injury. It is highly 
satisfactory especially in short bites and cupped out occlusals of filling, 
and also where two molars are unsupported on either side. 



612 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

The technic is as follows: Cut a deep trench mesiodistally in the 
filling selected for anchorage and a shallower one in the adjoining 
filling or, if necessary, grind a shallow polished groove in the occluso- 
proximal enamel. Roughen the wire where it is to be imbedded and 
shape and polish the projecting end with reference to its bed and the 
occlusion. Line both grooves with very soft amalgam. Tap the wire 
to a proper seating, cover with soft amalgam and harden by the 
wafering process. Uncover the occlusal of the projecting wire. When 
the amalgam has fairly set, move the teeth apart slightly to disturb 
any amalgamation of the projecting portion which should play in an 
adapted groove. 

This condition frequently results when a bridge has been inserted 
from a second molar forward. The third molar moves away. If 
any looseness of teeth exist it may be better to include the third 
molar as an abutment. 

Fig. 579 




Pin embedded in filling in third molar and extending into a groove in filling in 
second molar. Extension plays back and forth but protects gum. 



A further possibility lies in the use of a crown on the third molar 
with a hook or mortised piece attached, which hook or mortise plays 
in a suitable pocket in the crown attached to the bridge, or the pin 
referred to may play in a groove. Some cases of bridge work are 
constructed with hook attachment, said hook playing in a specially 
made inlay in a tooth not otherwise included in the bridge (Fig. 
579). 

Any associate pyorrhea due to this cause is usually rapidly cured 
by this establishment of contact, but may require some treatment. 

Following mechanical corrections perfect cleansing of all teeth is 
indicated, this to be maintained by monthly prophylaxis, at least 
until the case is cured and then continued periodically for prevention. 

In case of hypertrophic ulitis due to and covering a pontic tooth 
a mucous anesthesia is done and a semilunar cut made to carve off 



MARGINAL GINGIVITIS 613 

a piece of gum. The tooth is then cut down with a cone-shaped 
Miller carborundum stone and dressed smooth with abrasive strips. 

Waas, 1 by careful test, has found iodin trichlorin in 1 to 1000 
aqueous solution with menthol and saccharin added for flavor as 
destroying malignant streptococci and B. diphtherise in three minutes. 
It may therefore be considered first if active germicidal work is a 
necessity. 

Antiseptic mouth washes should be employed frequently, no 
matter what the cause. If the gum tissue be soft and spongy, 
showing signs of venous hyperemia, antiseptic astringent mouth 
washes should be freely used: 

1$ — Zinc, chlorid gr. x 

Aquae menth. pip fgj — M. 

Increase as desired. 

The above preparation, used in spray from an atomizer, or, if 
diluted, as a wash several times a day, is an excellent local application, 
meeting both indications. Prescriptions containing eucalyptus and 
benzoic acid are excellent: 

]$ — Acid, benzoic 3 parts 

Tinct. eucalyptus 15 parts 

01. menth. pip 1 part 

Alcohol 100 parts 

Saccharin 2 parts — M. 

(Miller.) 

The above formula diluted one-half is agreeable and efficient. 
An alkaline 1 per cent, salicylic acid wash is useful, not only for 
the gingivitis, but any attendant fetor of breath: 

1$ — Sodii boratis 3iss 

Acidi salicylici ...... gr. xv 

Aquae menthse pip f Siij — M. 

The following is astringent and antiseptic: 

Ifc — Boroglycerini, 

Tinct. krameriae, 
Tinct. calendulae, 

Alcoholis aa fgj — M. 

Sig. — One or two teaspoonfuls to a small glass of water. 

Truman advises the use of hydronaphthol in an astringent vehicle 
as an effective germicide for use by a patient: 

Ifc — Hydronaphthol gr. x 

Glycerol fgj 

Alcohol f 5j 

Aquae destil f5j — M. 

Sig. — Use as a wash several times a day. (Pierce.) 

1 Dental Items of Interest, March, 1918. 



614 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 
Talbot recommends for gingivitis the following : 

I^ — Zinc iodid 15 grams 

Iodin 25 grams 

Glycerin 50 grams 

Water 10 grams — M. 

Sig. — Apply to gum on cotton wound on an applicator and dry after each 
painting. (Talbot. 1 ) 

The writer has found this applied as directed and also diluted to 
one-fourth strength with water and applied frequently, by the 
patient as a lotion or approximately 1 to 100 as a wash to be very 
valuable in simple and suppurative gingivitis. It, however, causes 
superficial discoloration of the teeth and gives a leaden color to 
bridge-work as does iodine in any form. 

The following is a 5 per cent, formaldehyd solution which, diluted, 
can be used as a mouth wash, having astringent and antiseptic 
qualities. It is also useful in various strengths as a germicide for 
root canals. A formula for quantity is given, which may be reduced 
in prescriptions: 

No. 1 

3— Thymol 3iss 

Menthol 5ss 

Oil of ecucalyptus, 
Oil of gaultheria, 
Oil of cassia, 

Oil of cloves aa f 3iss 

Alcohol fgij — M. 

No. 2 

Formaldehyd, 40 per cent, sol Oj 

Boric acid, 

Sodium biborate aa 3iij 

Water Oij— M. 

No. 3 
Water to gal. j 

Make up No. 1 first and shake well. Place No. 2 in a gallon 
demijohn and shake well; add No. 1 and shake again; add No. 3 
and shake well. For dispensing this may be filtered; for office use 
this is not necessary. For mouth use one-half teaspoonful is to be 
diluted in two ounces of water, making a 1 to 600 formaldehyd 
solution. 

Equal parts of Listerine and ordinary distillate of hamamelis is a 
useful combination. Glycothymolin is a very popular proprietary 
mouth wash. Lavoris and Vernas Lotions are agreeable zinc chloride 
washes when used as directed. Phenol-sodique, 1 to 7 of water 
is quite useful. Alcohol 1 vinegar 1 water 8 is recommended. 

1 Dental Cosmos, 1905, p. 1312. 




MARGINAL GINGIVITIS 615 

For mercurial gingivitis and stomatitis the following has been 
rationally recommended i 1 

ty — Tinct. myrrhse f 3hj 

Potassii chloratis 3ss 

Sodii chloridi 3ij 

Aquae dis. . • q. s. ad f 5viij — M. 

Sig. — Use as mouth wash. Repeat every two hours. 

Fig. 580 

-r- ■ ■■ - *» ,."'- . .. •• 
St -..""" '. 

Showing Vincent's bacteria (the fine spiral forms). (Lederer.) 

All mouth washes require an application of about two minutes' 
duration at least twice a day after cleansing the teeth in order to 
produce the best effects. As this is somewhat fatiguing to the orax 
muscles, several applications may be made, one after the other 
until the total is attained (Fig. 580). 

In Vincent's angina (and in all acute suppurative conditions) I 
have found the following a very active germicidal wash: 

1$ — Hydrargyri bichloridi gr. j 

Aquae hydrogenii dioxidi f5iv — M. 

Sig. — Use several times a day. 

Vaughn 2 recommends silver nitrate 15 to 30 grains, water fgj, 
Lugol's solution, chromic acid 10 per cent., zinc chlorid 2 per cent., 
and argyrol full strength. Lederer applies salvarsan to the germs. 

1 Medical Press, via Dental Cosmos. 

2 Dental Cosmos, 1912, p. 655. 




610 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

Campbell and I has, 1 working on 129 cases in army service, use a 
routine treatment of liquor potassii arsenitis swabbed on three or four 
times a day. When ulcers are deep 10 per cent, silver nitrate is 
liberally applied and the above routine employed. Curettement is 
sometimes necessary. They use large doses of liquor arsenicalis inter- 
nally, sodium cacodylate hypodermically or salvarsan (in cases of 
general stomatitis and gingivitis) combined with antiseptics locally 
until the case is under sufficient control for the local treatment. The 
cure is in from four to seven days. Kirk 2 recommends in addition 
local application of tincture of iodin and irrigations of hot water. 
The glandular enlargements require a cold compress or the ice-bag. 
For the restoration of gum tissue between molars and bicuspids 
L. Ashley Faught 3 has recommended applications of 10 per cent, 
trichloracetic acid on an orange-wood stick every day or two until 
the case is cured. 



DEEPLY SEATED GINGIVITIS 4 (INTERSTITIAL GINGIVITIS, 

TALBOT). 

Definition. — This may be defined as an inflammation characterized 
by the presence in the deep connective-tissue elements of the peri- 
cementum and gum tissue of an excessive number of leukocytes, 
attracted thither by a general or local irritation of the tissue men- 
tioned. 

Local Causes. — Any of the local causes producing marginal gin- 
givitis, if acting deeply, may produce a deeply seated gingivitis. In 
addition to these, the eruption of teeth, the wedging of them, or 
their movement in orthodontia, the overuse, malocclusion, or dis- 
use, in short, any of the causes of pericementitis, septic or non- 
septic, if producing inflammation extending beyond the confines of 
the pericementum, are causes of deeply seated gingivitis. The simple 
inflammations are more liable to cause resorption of bone without 
loss of pericementum at the gum margin while the septic varieties 
are usually extensions of infective conditions from the gum margin. 
Pyorrhea alveolaris is a destructive, deeply seated gingivitis and 
pericementitis combined. Ulceration and necrosis following extraction 
cause gingivitis (see page 607). 

1 For their complete article and different varieties, see Jour. Am. Med. Assn., June 2, 
1917, and synopsis in Dental Cosmos, 1917, p. 838. 

2 American Text Book of Op. Dent., p. 300. 3 Dental Cosmos, 1905. 

4 The writer has introduced the term to replace interstitial gingivitis, not to multiply 
terms, but because it indicates fairly the anatomical situation. Strictly speaking, 
all inflammations are interstitial. 



DEEPLY SEATED GINGIVITIS 



617 



If at any time pyogenic infection occur at the gum margin, the 
purulent phenomenon of pyorrhea alveolaris is produced. It is to 
be understood that deeply seated gingivitis presents many of the 
features of pyorrhea alveolaris and that the latter is a gingivitis. 
The conditions are, however, pathologically separable. 

The following is a good example: A lady presented an upper 
first molar which had had a pyorrhea which had been cured by 
treatment of gum margins and the mesiobuccal root amputated. 
There was no longer any appreciable pus pocket, but the tooth 
overoccluded one-sixteenth inch and had tipped forward. It was 
not supported mesially or distally by adjoining teeth. It was loos- 
ened. The overocclusion was removed by grinding, the tooth was 
wedged against its mesial neighbor, and a distal amalgam filling 
contoured out to its distal neighbor, thus affording support in the 
direction of its movement in mastication. It became much firmer. 

Fig. 581 




Interstitial gingivitis on molars. 

The writer considers this case as presented for diagnosis one of 
deeply seated gingivitis due to non-septic pericementitis due to mal- 
occlusion and non-support, and not a case of pyorrhea. In like 
manner each case should be considered on its own symptoms. 

When food enters the interproximal space owing to faulty contact 
it crushes the gum septum and later depresses it. The inflammation 
causes its absorption as well as often that of the bone septum, so as 
to leave the buccal and lingual portion higher, forming a large open 
pocket for retention of food. This may also be inflamed and further 
depressed. The pericementi of both teeth suffer necrosis to the 
gum level. The pocket may finally suppurate and a lateral abscess 
may result from this cause called a septal abscess. 1 (For Marginal 
Abscess, see page 609.) A wide natural space between teeth does 
not generally produce this condition. 



Black. 



618 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

While this may be classified with pyorrhea alveolaris it seems to 
the writer rather a distinct form of deeply seated gingivitis, at least 
until the pus flow is established. The writer has seen another form 
of this condition in which caries at the linguocervical aspect of two 
molars permitted food to pack laterally (not from the occlusal) 
under tongue pressure. The decay proceeded up the sides of the 
lingual and buccal root adjoining, and a large pocket formed, the 
gum being stripped away. The wedging out .of the gum, touching 
with silver nitrate after cavity preparation, filling with amalgam., 
and polishing reduced the pocket to a simple one. The gum grew 
in as far as it could, and the part remains relatively healthy, without 
pyorrhetic symptoms, but food collects and the case in eight years is 
as in Fig. 582. In another part of the same mouth pus was found 
exuding from beneath the ulcerated flap of gum overlying a low T er 
third molar. Otherwise the patient's teeth exhibited no pyorrhea. 



Fig. 582 



Fig. 583 





Resorption probably starting with 
caries and continuing it (see text.) 



Remarkable case (bilateral) of root denu- 
dation. Note the bulge of the root, exact 
cause not known. (Kindness of a friend). 



Such cases might be considered pyorrhetic if pyorrhea is to include 
all pus flow^s from the alveolus, but then we must consider apical 
abscess such. The writer believes it better to differentiate the 
conditions. 

Systemic Causes. — Systemic causes act to produce a deeply seated 
gingivitis. Drug or metal poisoning, or auto-intoxication, whether 
gastro-intestinal or by leukomains, and acute infectious diseases, 
are systemic causes. (See page 572.) 

A case of spontaneous loss of all but one of the upper teeth, with 
subsequent complete alveolar atrophy as the result of the trophic 
disturbance from peripheral neuritis in a tabetic woman, has been 
reported by Gaucher and Dobrovici, the diagnosis being confirmed 
by trophic disturbance in the foot followed by plantar perforation. 

It seems quite certain that in conditions of general faulty metab- 
olism substances are generated in the system or are retained by 



DEEPLY SEATED GINGIVITIS 619 

reason of faulty elimination, and which, floating about in the blood 
stream, act as irritants to the pericementi and gum margins about 
the teeth. 

Moreover, the pericemental glands seem to be eliminating organs 
which may become overstimulated and thus diseased. 

In all general nutritional disorders parts peripheral to the circu- 
lation are most affected, become debilitated, and tend to a degener- 
ative metamorphosis of cells. 

As some proof of such an effect in another peripheral part a woman 
with apical granulomata had corrugated finger nails. Within two 
months of the removal of the teeth mild maniacal symptoms either 
concomitant with painful neuritis producing insomnia or caused 
by the abscesses has disappeared with the neuritis and insomnia 
and the finger nails are assuming normal shape. 

Rhein found, after repeated examinations of hospital patients, that 
"marginal gingivitis was an accompaniment of typhoid fever, tuber- 
culosis, malarial disorders, acute rheumatism, pleurisy, pericarditis, 
and syphilis, among the acute diseases. Of chronic nutritional dis- 
eases, it was commonly observed in cases of gout, diabetes, chronic 
rheumatism, several forms of nephritis, scurvy, chlorosis, anemia, 
leukemia, and pregnancy. Also in disorders of the central nervous 
system and following the administration of mercury, lead, and iodin." 

Rhein states that the gingivitis produced by each of these diseases 
has distinctive features which may even serve as diagnostic signs of 
the nature of the general malady. 

Talbot's experiments in the mercurialization of dogs (see page 568) 
demonstrate that efforts upon the part of the pericementum to elimi- 
nate the bichlorid of mercury result in a non-septic pericementitis, 
exhibiting in its morbid anatomy the characteristic round-celled 
infiltration of inflammation. 

Black 1 has shown that a gingivitis .produced by the systemic 
administration of potassium iodid may be proved to be caused by 
its elimination by the pericemental glands by test of the gingival 
secretion for the iodin reaction. 

It is quite reasonable to suppose that irritative substances origi- 
nating in the body and floating in the blood stream may act in like 
manner. This has been termed auto-intoxication. 

Irritation resulting from the administration of mercury, lead, and 
iodin, or from toxic substances absorbed from the intestines, is, of 
course, extrinsic intoxication, but acts in the same manner. 

It has been claimed by Hunter, Herschell, Goadby, W. B. Keyes, 

1 American System of Dentistry. 



620 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

D. D. Smith, and others, that the toxins formed by oral fermenta- 
tions and the septic infection of the stomach, intestines, etc., arising 
from the mouth are competent to excite a train of systemic dis- 
turbances ending in a general malnutrition (see page 557) . 

Certain accomplished cures of such states by treatment of acute 
suppurative conditions in the mouth and even constant oral pro- 
phylaxis lend plausibility if not certain proof to this argument. 
Still, the malnutrition, whatever its cause, oral or otherwise, may 
become a predisposition by lessening the resistance of the soft parts 
about the teeth to local irritants or add the irritation due to auto- 
intoxication. 

Talbot claims that interstitial gingivitis is largely due to auto- 
intoxication due to intestinal fermentation with production of by- 
products, notably indol, which, when absorbed, may or may not be 
eliminated through the eliminating organs — liver, kidneys, skin, and 
lungs — and that if these be insufficient to the task, retention occurs 
and even further disease of the organs themselves, especially the 
kidneys. Constipation aggravates the condition, if not producing 
it, by retention of fecal matter with which the poisons should be 
eliminated. The overstrain of the kidney in the endeavor to take 
up the work of the liver (when that is diseased) in elimination, 
produces renal inflammation and impairment of eliminative func- 
tion. 

The blood is surcharged with accumulated poisons, the heart and 
arteries degenerate, and cardiac hypertrophy and arteriosclerosis 
are produced. Blood pressure is increased and end artery and nerve 
degeneration occur, in the brain, eye, alveolar process, pulp, etc., 
being noticeable first in the gums. He draws attention to the transi- 
tory nature of the alveolar process and the inability of the arteries 
to expand, as in soft tissues, and that poisonous products settle in 
the end arteries, and points out that gingivitis is a natural result 
of these conditions. The demonstration of infarction in the pulp 
due to systemic conditions, even in the young, has been made by 
Hopewell-Smith, and also indicates end-artery strain. (See page 420.) 

Talbot regards indican, the absorbed product of indol in the 
intestine due to putrefaction and which is found in the urine, as the 
excitant of gingivitis in intestinal fermentation (auto-intoxication) 
and the general acidosis, as indicated either by an excess of acidity, 
in the urine or a deficiency therein, as excitant in various conditions 
of malnutrition. 

The excess of acidity above 40° in the urine indicates excessively 
imperfect oxidation, while defective acidity (below 30°) indicates 
insufficiency of renal elimination. In both cases systemic acidosis is 



DEEPLY SEATED GINGIVITIS 621 

the condition. To these views must be added the concept of intestinal 
putrefaction caused by oral infection progressing gradually toward 
establishment of a pyorrhea or deeply seated gingivitis. Thus the 
profession is divided into two schools: (1) Those who favor a sys- 
temic condition as a cause of pyorrhea, etc., and (2) those who regard 
a systemic condition as caused by oral infections. In view of the fact 
that a vicious circle is established, they are difficult to relate as to 
cause or effect in the beginning. Later they are no doubt interrelated, 
one predisposing to the other. 

Black's observations upon the origin of calculus in the blood (see 
page 632) shows a so-called systemic foundation for supragingival 
and subgingival calculus deposition and their ulterior local pathologi- 
cal effects resulting in gingivitis. 

Diagnosis of Systemic Causes. — The diagnosis of systemic cause 
by malnutritional conditions involves almost the entire range of 
medical diagnosis, a subject obviously beyond the scope of this 
work. If local causes do not explain the oral pathological condi- 
tion it is well to refer the patient to a competent medical diagnos- 
tician for examination and treatment. Urinalysis or salivary analysis 
may, however, be made by either the dentist or a specialist in that 
work, and together with symptoms some information may be gained. 
Talbot directs that twenty-four-hour urine should be obtained and 
the following points looked for. 1 

Amount. — This should be about forty ounces. 

Specific Gravity. — If high, it indicates an increased proportion of 
solids per ounce. 

Degree of Acidity. — If above 40° it indicates acidosis by imperfect 
oxidation; if below 30° it indicates renal insufficiency and retention 
in blood of acid products. 

Indican. — If present, it always indicates intestinal fermentation. 

Albumin. — Not of certain origin. 

Hyalin Casts. — If bloody, they indicate renal inflammation. 

Compound Hyalin and Coarsely Granular Casts and Waxy and Amyloid 
Casts. — Indicate changes in structure of kidney. 

Symptoms. — Headache, loss of appetite, loss of memory, irrita- 
bility, biliousness, fatigue, muscle soreness, hypochondriasis, in- 
somnia, vertigo, muddy complexion, tinnitus aurium, general ner- 
vousness, cold extremities, impotence, leg cramps, twitching of 
muscles, neurasthenia, pruritus, acne, urticaria, arteriosclerosis, gout, 
rheumatism, Bright's disease, diabetes, uric acid diathesis, nervous 
disorders, asthma, anemia, lethargy, stupor, insanity, etc., are 

1 Interstitial Gingivitis due to Auto-intoxication, Journal American Medical Asso- 
ciation and Dental Digest, 1906. 



622 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

symptoms which, in part, may develop from the auto-intoxication 
by the toxins and acidosis. 

Unnatural odor of the breath, armpits, and thighs indicate an 
effort of the lungs and skin at elimination. 1 

Lead poisoning occurs in those using white lead, as painters. The 
occupation together with paralysis of the extensors as in wrist or 
foot-drop, tremors, and peripheral anaesthesia from toxic peripheral 
neuritis and the blue lead line upon the gum are diagnostic points 
with which mercurial symptoms of like character may be confused 
though urinalysis for lead, the history and occupation clear it up. 

In mercurial poisoning the occupation, history of drug adminis- 
tration, salivation, enlarged tongue, general pericementitis or gingi- 
vitis, urinalysis for mercury, will clear the diagnosis as against 
that of lead poisoning. 

Bismuth subnitrate used in pastes for treatment of fractures, 
rilling cavities in bone, etc., has occasionally produced gingivitis by 
systemic intoxication. A bluish discoloration of the gums is noted. 



Fig. 584 



Fig. 585 



Fig. 5S6 






Resorption of alveolar process due to interstitial gingivitis, caused by marginal irri- 
tation from excessive filling material. (Radiographs by Price.) 

Pathology and Morbid Anatomy. — The local or systemic causes 
produce direct inflammation; the bloodvessels become overful, and 
waste products collected in the end arteries produce local degenera- 
tion, diapedesis of leukocytes into the interstitial submucous gum 
tissue occurs, and the spaces are filled with inflammatory exudate. 
The papillae become enlarged and the epithelial layer undergoes an 
increase in formation of cells (hyperplasia). The gum in consequence 
of these changes becomes swollen, its color deepened, and it bleeds 
readily. 

If the process be advanced the alveolar process is involved. 

After a time the effects of continued low-grade inflammation are 
expressed in resorption of bone or cementum, or hypertrophy of 



Talbot. 



DEEPLY SEATED GINGIVITIS 623 

bone or cementum, or both, as the two processes may be in evidence 
at the same time. 

Talbot describes several forms of bone resorption occurring in 
interstitial gingivitis : 

(a) Lacunar resorption carried on by the osteoclasts normally 
lying upon the surface of the bone. Under irritation they increase 
in number and excavate irregular bays in the bone (Howship's 
lacunae). These are then deepened and widened, destroying areas 
of bone. (See Figs. 17 and 564.) 

(b) Perforating canal resorption beginning in the small canals 
normally perforating the trabecule of bone in various directions and 
transmitting the bloodvessels from one medullary space or Haver- 
sian canal to another (Volkmann's canals). The osteoclasts widen 
these, necessarily reducing the substance of the trabecular (Fig. 15). 

(c) Halisteresis ossium, beginning with a decalcification of masses 
of the bone, the organic matrix being for a time undisturbed, but is 
later removed. This is a local expression of what may occur in other 
bones of the body in the condition known as osteomalacia (Fig. 18). 

According to Talbot, premature resorption of the alveolar margins, 
either local or general, is due to this process, called by him alveolar 
osteomalacia, and occurs in pregnancy or senility, as a rule. 

He states that the decalcified bone may be recalcified after con- 
finement in pregnancy, but is never restored in senility. 

A lesser degree of irritation may set the osteoblasts at work and 
cause the building up of the alveolar process, either as a restoration 
of resorbed bone or as an hypertrophy of either the alveolar process 
or the cementum of the root (hypercementosis) . 

Endarteritis obliterans is a thickening of the intima of an artery 
or capillary, due to chronic irritation, and causing a lessening of the 
lumen of the vessel, even to the point of obliteration of the capil- 
laries. 

The blood flow is impeded and nutrition of cells impaired. Any 
cause of deeply seated inflammation may produce it. In all cases 
of chronic deeply seated gingivitis the bloodvessels are so diseased 
(Figs. 587 and 588). 

Local Treatment. — The treatment must be directed to the removal 
of the underlying cause. All local causes must be removed and the 
teeth put into physiological use as far as possible. This includes 
the removal of causes of malocclusion or overuse; of the crowding of 
food between teeth, the removal of local mechanical irritants and 
infective agents. The local treatment in general is that employed 
for marginal gingivitis or for pyorrhea alveolaris. (See page 610; 
also Pyorrhea Alveolaris.) 



624 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

Systemic Treatment. — This, of course, depends upon the systemic 
condition and its causes, but if due to torpid biliary function or 
defective elimination with consequent retention of body products, 
the restoration of the eliminative function should be aimed at. In 
intestinal auto-intoxication, impacted fecal matter should be removed 
by repeated injections, if necessary, of warm water, and the bowels 
be kept clear by flushing with soap and water once or twice a week. 
The bile function should be restored, and the bile be increased 
in flow by calomel and soda, T V to J gr., every hour until 1 grain 
is taken; to be followed by a saline laxative (as Seidlitz powder); or 
podophyllin, ^ to "J gr., up to \ gr., may be given instead of calomel. 

Fig. 587 Fig. 588 






*atf£»^ -k 


>.j£| 






NcS.~-. 




'lfe> 




-"" -"--i -w. ' Wi* - 








' )) 


- A % 






—-—J^^&S^t' 




-^gSpF-/ 




1 



Fig. 587. — Longitudinal section of gingival border, showing round-cell inflamma- 
tion, due to mercury, and extending to the inner coat of the bloodvessel, and also 
plasma mast cells. From a dog. (Talbot.) 

Fig. 588. — Endarteritis obliterans: A, adventitia; E, elastic tissue between middle 
coat and intima; M, muscular coat; /, thickened intima. (Talbot, after Kaufmann.) 

Talbot 1 also uses: 

]$ — Aloin | gr. 

Strychnin sulphate -^ gr. 

Extract of belladonna £ gr. 

Pulv. ipecac -^ gr. — M. 

Take at bedtime and follow with a saline cathartic next morning. 
If the stools remain unhealthy, administer each two to four hours 2 
to 5 grs. of compound lime, soda and zinc carbolate until the stools 
are healthy. 

1 Therapeutics and Treatment of Interstitial Gingivitis, Dental Digest, 1906. 



MARGINAL ATROPHY OF THE GUMS 625 

To continue the stimulation of the liver administer bilin tr to 
i gr. four or five times a day. 

The constant use of heavy liquid white petrolatum, for the purpose 
of clearing the intestinal mucosa, by lubrication is valuable. Mas- 
sage of the abdomen restores the tonicity of the bowels. 

The urine should be examined for evidence of established disease, 
and if this be found the patient referred to a general practitioner. 
(See General Malnutrition.) If found only symptomatic of hepatic 
or renal insufficiency and nutritional disorder, the amount of urine 
should be increased to 40 ounces by the drinking of 3 pints of water 
(including table beverages) per day, which will aid bowel and renal 
elimination and flush tissues of accumulations, including retained 
acids. If the urine be abnormally acid (above 40°) administer 
3-gr. tablet of lithia, sodium bicarbonate, or sodium chlorid in a glass 
of water four times a day. Hot or Turkish baths keep the skin 
free for eliminative function. Well-apportioned rest and exercise 
and moderate eating of proper nutritious food are indicated. When 
organic disease is present the treatment should be relegated to the 
medical practitioner. 

MARGINAL ATROPHY OF THE GUMS. 

In advanced age there exists often a tendency of the gums to 
shrink evenly away from the enamel, exposing the cementum. Hope- 
well-Smith describes this as accompanied by fibroid degeneration 
of the pericementum (which see), and regards the latter as a purely 
senile change. 

In discussing the alveolar conditions antecedent to pyorrhea 
alveolaris he describes a resorption of marginal and radicular bone 
of the halisteritic type followed by lacunar resorption extending 
finally into perforating canal resorption which constitutes an osteo- 
porosis 1 (see page 623). The alveolar process is gradually lost. In a 
later paper 2 he gives the following reasons for marginal atrophy in 
senile (or precocious senile) conditions: (1) The thinness of the alveo- 
lar margin with few Haversian canals and medullary spaces and con- 
sequent inadequate blood supply and tendency to malnutrition and 
atrophy. (2) Its practically functionless character due to lack of 
muscular attachment. This idea is elaborated by Roy 3 who claims 
that senility and precocious senility due to causes associated with 
the vitality and general nutrition of the individual (especially arthrit- 
ism) is the systemic cause of the local condition, quoting Bell, DeBois, 

1 Dental Cosmos, 1911, p. 405. 2 Ibid., May, 1918. 

3 Ibid., 1918, p. 761. 

40 



620 PERICEMENTAL DISEASES BEGINNING AT GUM MARGIN 

Talbot and Baume as previous observers. The condition seems 
inseparable from pericemental degeneration as an associated process. 

It may be noted upon the buccal side only of a denture, and be 
due to vigorous brushing. 

It is also seen localized at cervices next to a space from which a 

tooth has been extracted. In one case the editor saw a slightly 

hypertrophied gum distinctly overlapping a cavity margin drawn 

back one-eighth inch within a month as the result of extraction of the 

adjoining root. 

Fig. 589 




Recession of gum in senility; beginning decalcification of cementum; alveolar resorp- 
tion after extraction. (Philadelphia Dental College Museum.) 

It may be that collections upon the teeth are in some degree 
responsible. The gums have, for the most part, a healthy look, but 
are in a condition predisposed to pyorrhea alveolaris. 

Treatment. — The treatment of a general tendency of this sort is 
stimulation. Brushing, use of the foods requiring mastication, 
massage and Bier's hyperemia by suction. (See Treatment of Pyor- 
rhea for ideas.) If localized to a particular tooth and the restoration 
of the gum be desirable, Harlan's method may be tried. 1 (1) Cleanse 
the exposed tooth surface and slightly roughen it near the gum 
margin. (2) Dissect away the gum from the root to about one- 
quarter inch in depth, wiping the blood away carefully with mouth 
open until hemorrhage ceases spontaneously, or check with adrenalin 
solution. (3) Make three incisions into and through the gum tissue. 

■ Dental Cosmos, 1906, p. 927, and 1907, p. 598. 



MARGINAL ATROPHY OF THE GUMS 627 

(4) When bleeding has almost ceased fill the cuts with dried zinc iodid, 
allowing the blood to liquefy it so that it may be carried around 
the gum margin. This creates a profound irritation, which should 
not be disturbed. (5) The patient should use a mild antacid anti- 
septic wash, as of sodium bicarbonate or milk of magnesia. (6) Re- 
peat three or four times at intervals of three or four weeks, with 
cuts in a new location. (7) Use silk or pure silver ligatures around 
the teeth under the gum for further irritation. (8) To allay over- 
irritation paint with 1 part adrenalin and 3 parts compound tincture 
of iodin once in three days. 

Harlan states that a long time may be required in some cases. It 
should not be attempted over a gold filling, but an unglazed porcelain 
may be covered, though no attachment will exist. The principle 
involved is that of coaxing the gum into adherence with the roughened 
root, and the filling in of the cut with scar tissue. 

As a wash use: 

1$ — Hydronaphthol gr. xx 

Oil eucalyptus TTtx 

. Oil cassia ttlx 

Alcohol f 3iij 

Distilled water f3xiij — M. 

Sig. — Use freely five or six times daily, diluted, if necessary, with more water. 

The gums should not be brushed for several days after operating. 
Avoid insoluble dentifrices. If this treatment be considered inad- 
visable the appearance in a given case may be improved by the 
use of a pink or partly pink porcelain inlay. 

For general recession due to osteomalacia the general acidosis 
may be treated (see p. 624). 



CHAPTER XX. 
SALIVARY AND SERUMAL CALCULUS. 

Calculi are more or less hard concretions found in varying situa- 
tions and composed of inorganic and organic matter combined in an 
unknown manner. 

As related to the teeth, calculi arise from the following recognized 
local sources: 

1. Obviously from the saliva, and deposited in situations which 
clearly indicate its source, salivary calculus (or ptyalogenic calculus 
— Peirce). 

2. From the serum of the blood deposited at some point along the 
side of the root between the gum margin and' the apex of the root, 
and called serumal calculus (Black), or sanguinary calculus (Inger- 
soll). Of this there are several varieties: 

(a) That associated with a probable fermentation and an altered 
secretion from the gum margin, and known as subgingival calculus. 

(6) That occurring in situations in which a chronic pus flow is 
found, whether apical or subgingival, and which may be called 
pyogenic calculus. 

(c) That found upon the roots of teeth at a point to which saliva 
has no access and over which pus does not flow, and which is there- 
fore deposited by the lymph derived from the blood, and to which 
the appellation hematogenic calculus (Peirce) is applicable. 

In this class Kirk found two varieties resulting from pericemental 
inflammation: (1) Subpericemental deposits, and (2) intraperice- 
mental deposits. 1 

These several names will be adhered to in further descriptions as 
having definite significance. 

The experiments of the late Dr. Black seem to indicate that all 
these deposits are explainable upon the evidence tending to show 
that calculus is a finely divided calcoglobulin formed into spherules 
in the blood and thrown into any location which favors its deposit. 
Apparently they therefore have a common origin in the blood. 

SALIVARY CALCULUS. 

Definition. — Salivary or ptyalogenic calculi are hard formations 
composed mainly of calcium salts combined with organic substances, 

1 Dental Cosmos, 1905. 

( 028 ) 



SALIVARY CALCULUS 



629 



probably a globulin or globulins into minute spherules of calco- 
globulin which have been deposited in a soft state from the saliva 
upon the teeth or other objects in the mouth and have hardened in 
the locations where deposited. 

Occurrence. — They are found upon the surfaces of the teeth, 
notably in situations opposite the mouths of the salivary glands, in 
the ducts of the muciparous salivary glands (sublingual and sub- 
maxillary), and upon artificial dentures. A photograph of a plate 
containing an enormous mass of calculus, the result of seven years' 
accumulation, is shown in Fig. 590. The teeth are occasionally 
buried in it. The editor extracted three lower incisors which had 
been wired together, and were absolutely covered from the neck to 
the apex by calculus (Fig. 591). 

Varieties. — Clinically two distinct varieties of salivary calculus are 
recognizable: (1) The soft, friable, whitish yellow deposits found 
chiefly upon the buccal surfaces of the upper molars and upon 

the lingual surfaces of the lower 
FlG - 590 anterior teeth; (2) dark-colored 

and hard deposits found more 
frequently in the latter situation, 
less frequently in the former. 

Fig. 591 




Salivary calculus attached to a lower 
partial plate worn seven years without 
removal. Shows form of sublingual 
space. Practice of Dr. Ford, Toulouse, 
France. (Specimen in possession of 
Philadelphia Academy of Stomatology.) 




Teeth lost by salivary calculus formation 
(see text). 



Origin of Salivary Calculus. — The origin of salivary calculus 
may be studied from several standpoints: (1) The formation 
of calculi in other parts of the body; (2) an analysis of saliva 
and salivary calculi; (3) extra-oral experiments upon saliva 
with a view to the formation of salivary calculus extra-orally ; 

(4) observations upon saliva taken directly from the salivary duct ; 

(5) the changes observed clinically in salivary calculus during its 
deposition. 

1. Ziegler 1 states that all free concretions have an organic basis 



General Pathology. 



630 SALIVARY AND SERUMAL CALCULUS 

or nucleus (inspissated feces, vegetable material, epithelial scales, 
mucus, etc.). 

As to cholesterin gallstones, he states that if the cholesterin be 
dissolved out by ether, a yellowish organic matrix remains which 
retains the form of the stone and presents upon examination radiating 
spaces formerly occupied by the crystals. He describes the forma- 
tion of the gallstone as an infiltration or incrustation of degenerated 
organic matter (epithelial scales, etc.) with cholesterin, bile pigment, 
etc., to which, after a nucleus is formed, other portions are added in 
like manner. 

Of urinary calculi he states that Ebstein has shown an organic 
substance albuminous in nature to be left after dissolving out the 
various salts. 

In stratified calculi this stroma also shows stratification. Such a 
stroma may be seen after decalcification of a bit of salivary 
calculus. 

Calculi are also deposited in the walls of degenerated arteries and 
in degenerated tissue in general as in tumors or in the pulp tissue 
(see page 62) . The conditions simply favor its deposit from the blood 
as calculus (calcoglobulin) or it is possible that a reaction occurs 
between the albuminous elements of the degenerative tissue and the 
calcium salts in a sluggish lymph. Foreign bodies imbedded in the 
tissues or excretory passages may also have calculus upon them, as 
encysted bullets (Black) or objects in the bladder. 

2. Analysis of salivary calculus shows it to be composed of about 
22 per cent, of water and organic matter as the portion removable 
by burning the calculus, and about 78 per cent, inorganic matter as 
the portion removable by decalcification with acids. 

Following are the analyses of salivary calculus by Stevenson and 
Schehevetskey, respectively : l 

Soft tartar Hard tartar en 

on molars. lower incisors. 

Water and organic matter 21.48 17.51 

Magnesium phosphate 1.31 1.31 

Calcium phosphate with a little carbonate and 

trace of fluorid 77.21 81.18 

100.00 100.00 

Water and organic matter 22.07 

Magnesium phosphate 1 . 07 

Calcium phosphate 67.18 

Calcium carbonate 8.13 

Calcium fluorid 1.55 

100.00 
1 Talbot. Interstitial Gingivitis. 



SALIVARY CALCULUS 631 

These observers are practically agreed upon the substances present 
in calculus as mainly calcium phosphate with some calcium carbonate, 
calcium fluorid, and magnesium phosphate combined with organic 
matter. 

Talbot furnishes the following analysis of serumal calculus by 
J. H. Salisbury: 1 

Water and organic matter 32 . 24 

Magnesium phosphate . 98 

Calcium phosphate . 63 . 08 

Calcium carbonate 3.70 

100.00 

To these Kirk 2 adds ammoniomagnesium phosphate as a product 
of putrefaction. 

According to Mitscherlich, 3 parotid saliva contains globulin, but 
no mucin, and contains calcium carbonate; calcium phosphate being 
present in but minute amount. The submaxillary saliva contains a 
large amount of mucin, which gives to mixed saliva its viscid nature. 

Analyses of submaxillary saliva and mixed saliva by Bidder and 
Schmidt gave the following results: 

Submaxillary Saliva. 

Water 991.45 

Organic matter 2.89 



Inorganic matter 



Calcium chlorid 
Sodium chlorid 



4.50 



Calcium carbonate 

Calcium phosphate } 1 . 16 

Magnesium phosphate 



1000.00 



Mixed Saliva. 

Water 995.16 

Epithelium 1.62 

Soluble organic matter 1 . 34 



Organic matter 



Potassium suiphocyanid 0.06 

Inorganic matter \ Sodium, calcium, and magnesium phosphate 0.98 
Sodium and potassium chlorid . . . 0.84 



1000.00 



That an error of experiment or estimation exists in these analyses 
is shown by the fact that calcium carbonate is not mentioned as 
existing in mixed saliva, while it exists in submaxillary saliva; this 
is a physical impossibility. 

1 Talbot. Interstitial Gingivitis. 

2 Dental Cosmos, 1905, p. 752. 

3 Halliburton. Physiological and Pathological Chemistry. 



632 SALIVARY AND SERUMAL CALCULUS 

It is presumptive, however, that calcium carbonate has not been 
specially estimated. 

If a bit of calculus be dried and then burned at a red heat, the 
organic matter present will burn out, the calculus retaining its form. 
If a similar bit be subjected to dilute acid (1 per cent, nitric) the 
inorganic matter will be removed, the calculus will float to the top 
of the liquid, and, after a time, remain as a light stroma of nearly 
the original form of the piece. 

If a bit of calculus be transversely ground; it is seen under a low- 
power lens to present a laminated appearance — i. e., it has been 
deposited in layers representing periods of activity. The under 
surface of the calculus shows a concentric formation. Beneath the 
mass a nidus of darker calculus may be found, and if section of 
extensive calculi be made the greenish deposits may be seen scattered 
through the mass. Black has noted the presence of urates in nearly 
all specimens examined by the murexid test. Foreign bodies are 
sometimes entangled in the mass. Peirce recorded a case in which 
a small clasp plate was securely fastened to the teeth, and the patient 
denied possession of such a substitute (see also Fig. 591). 

In some cases extensive salivary deposits are found associated 
with highly offensive odors — i. e., putrefaction of the organic matter 
occurs as a part of the process — indeed, bacteria are constantly 
associated with the mass and may furnish their quota of the organic 
matter. Extraneous matters, such as tobacco smoke or other pig- 
ments, cause discoloration of the mass. With data relative to the 
physical and chemical analysis of calculi, the mode of calculus forma- 
tion may be studied. 

3. If a test-tube be filled with saliva and allowed to remain at rest 
for several days, a flocculent, light yellow precipitate will be noted 
at the bottom of the tube. If the supernatant fluid be drawn off 
with a pipette and the precipitate be allowed to dry, it will be found 
possessed of the chief characteristics of calculus — hardness, friability, 
a light yellow color, tenacity of adherence to objects with which it 
is in contact, and capability of analysis into organic matter and 
inorganic salts. 

4. Dr. Black's studies 1 have established the following important facts : 
(a) That minute spherules of calcoglobulin may be collected from 

saliva drawn into test-tubes direct from Stenson's duct by means of 
a canula and that therefore it is not necessarily dependent upon 
oral conditions. As the saliva was found sterile the combination is 
not necessarily due to microorganisms. 

1 Text-book Special Dental Pathology. 



SALIVARY CALCULUS 



633 



Fig. 592 




A, nidus; B, calculus. 



(b) That the deposits are paroxysmal in character, being found to 
take place only for a limited time and not appearing in the saliva 
of the same individual before or after the period of deposit and that 
the period of the "shower" may vary from a half hour to several 
hours. 

(c) That the paroxysm was dependent upon the quantity of nutri- 
tious food taken at a meal rather than the quality of it. That full 
meals would induce it while a half meal would not. 

(d) That persons in ill health due to digestive disturbances might 
have no calculus owing to non-assimilation of food while others in 
"a low state of health" might 

have the organic portion, globulin, 
called by Black " agglutinin of cal- 
culus" without calcium salts in it. 

(e) That examined on cover- 
glasses specially arranged to catch 
the soft calculus entering the 
mouth the spherules may be 
specially stained and examined 
microscopically with the finding 
of several varieties reacting differ- 
ently to stains indicating that the agglutinin base may vary in its 
albuminous composition and in the amount of calcium salts in the 
combination. 

(/) That on plates the mucous coating could be washed off in 
running water while the calculus could not, but that it could readily 
be removed with a brush and water if fresh, but that if twenty-four 
hours old it has begun to harden and is difficult of such removal, and 
after several days cannot be so removed. 

(g) That he was unable to separate the calcoglobulin into its 
components without destroying them which means probably a firm 
chemical combination. 

He suggests the tentative theory that overeating creates an excess 
of globulin or globulins in the blood which when in variable over- 
accumulation are thrown out with secretion or excretions probably 
in combination with calcium salts as spherules of calcoglobulin which 
in the mouth deposit first as a soft mass which then hardens by 
decomposition of the colloid elements. He also concludes that the 
serumal deposits have a similar origin. 

The blood contains about 0.8 per cent, of inorganic salts, including 
those found in salivary calculi, and a certain percentage of them is 
also found in the blood corpuscles. They probably, therefore, exist 
in body cells in some proportion. 



634 



SALIVARY AND SERUMAL CALCULUS 



The salts are also taken into the body in the form of food. Their 
appearance in the various excretions and secretions of the body is to 
be regarded as in all probability an effort upon the part of the system 
to eliminate a superabundance of inorganic material from the body. 
They are therefore in readiness for combination with globulin in the 
blood. 

The ingestion of quantities of animal or of vegetable food rich 
in phosphates, or the excessive liberation of the phosphoric acid in 
malnutrition, may produce an excessive elimination of these in 



Fig. 593 



Fig. 594 




Unclean necks of teeth, salivary calculus, 
and green stain. (Philadelphia Dental Col- 
lege Museum.) 



A, maxillary sinus; B, duct of Steno; 
C, parotid calculus; E, submaxillary 
gland. 



the excretions and cause a tendency to the production of calculi 
about the body. This condition, known as phosphaturia, is observed 
in certain nervous diseases, rachitis, osteomalacia, leukemia, gout, 
and rheumatism, 1 in which the phosphaturia is symptomatic of an 
excessive katabolism; also in intestinal disturbance resulting in 
imperfect assimilation of food. 

Whether taken in as food or liberated during metabolism it is 
probable, as pointed out by Talbot, that if one excretory organ fail 



Thompson. Practical Medicine. 



SALIVARY CALCULUS 



635 



to perform its office in full degree another must take up its work. 
For these reasons, in any bodily condition affecting elimination a 




S.L.3.L 

C, calculus; S.L.C., sublingual cavity; S.L.GL., sublingual gland. 

superabundance of inorganic salts and globulin may appear in the 
blood and hence in the saliva, and, probably, in even the secretions 
from the gingival margins. 

Fig. 596 




Right side, abrasion from overuse; left side, deposits due to stagnation. 



That the deposit of calculus may have some dependence upon the 
superabundance of calcium salts in the system is evidenced by the 
fact that in young children but little calculus is deposited upon the 
teeth. The salts are needed in bone formation. 



636 SALIVARY AND SERUMAL CALCULUS 

5. That rest or relative quiescence of the saliva is favorable for the 
localization of calculus is shown by the fact that it occurs at points 
which are ordinarily not subjected to agitation — i. e., buccal surfaces 
of upper molars, lingual and labial surfaces of lower incisors. 

Adhesive precipitations of newly formed and very soft calculus 
form in these latter situations in the course of the day. If not removed 
by brushing they harden and thicken. An unused side of a denture 
often accumulates calculus in greater degree than the side used for 
mastication. This does not occur, however, if the brush be used 
properly and equally vigorously upon both sides. 

In the analyses furnished by Stevenson (p. 630) it will be seen 
that hardness is, in part at least, due to an increased proportion of 
inorganic elements. 

Fig. 597 - Fig. 598 





Section of a lower incisor, with a large Section of an upper molar with deposit 

deposit of salivary calculus impinging of calculus on its buccal surface, causing 

upon and causing inflammation of the inflammation and absorption of the gum 

gum. (Black.) and lower border of the peridental mem- 

brane and alveolar wall. (Black.) 



Pathological Effects of Salivary Calculus. — In contact with the 
mucous membrane a salivary calculus excites first marginal gingivitis, 
and later deeply seated gingivitis and its effects. There is sometimes 
in this stage the wavy, gnawing, uneasy sensation, associated with 
mild inflammation, and the pulp being supplied with excess blood, 
becomes hyperemic and the teeth respond more readily to thermal 
stimuli. (See p. 383.) The gum margin is inflamed, and occasion- 
ally pyogenic organisms cause pus formation. The gum margin 
recedes and coincidently a resorption of the alveolar process is 
produced. More calculus is deposited and the process proceeds 



SALIVARY CALCULUS 



637 



until much of the alveolar support is lost. Microorganisms no doubt 
aid in the process (see Fig. 600 and page 590). 

The tooth is thus progressively loosened, first by inflammation ; 
later by loss of alveolar process, moves about, and a resultant mechan- 
ical non-septic pericementitis occurs; as a result the membrane is 
thickened and the alveolar process partially resorbed (Fig. 597). 
As soon as the alveolar loss is considerable, infection usually occurs 
and suppuration may be grafted upon the results of mechanical 
irritation. Increased looseness occurs until the tooth drops out, 
unless mechanically held in place. 



Fig. 599 



Fig. 600 





Section illustration of a heavy deposit 
of salivary calculus on a lower incisor, 
with partial destruction of the alveolus 
of the tooth. (Black.) 



Sectional illustration of lower in- 
cisor, with deposit of salivary cal- 
culus less heavy than that shown in 
Fig. 599, but with greater destruc- 
tion of the alveolus. (Black.) 



The entire process may occupy but a few years; in other cases 
the atrophy of the alveolar walls is very slow. I have recently seen 
a case like that shown in Fig. 599 on about eight lower teeth. The 
patient had not consulted a dentist for thirty years. During the 
following three years but little accumulated. The patient has in 
the meantime suffered from a severe form of heart disease and his 
low diet may explain the absence of calculus (as per Black's theory 
of calculus formation, page 634). 

It has been shown that in more advanced cases and even in some 
of the simple ones that salivary calculus and its associate putre- 
factions may be a cause of systemic infection as in the case of pyorrhea 
alveolaris, some of these clearing up upon the establishment of normal 
oral cleanliness. (See Systemic Effects of Pyorrhea.) 



638 



SALIVARY AND SERUMAL CALCULUS 



Prognosis. — The prognosis of this condition depends upon the 
extent of alveolar atrophy. If the loss of support be not so extensive 
as to cause marked loosening of the tooth or teeth, the teeth may 
be retained for an indefinite period if they receive constant prophyl- 
axis. If markedly loosened they must be splinted so as to render 
them firm. If left unsupported, the pericementum is certain to 
degenerate, owing to the increased mobility. The alveolar atrophy 
will continue, and probably infection of the degenerated pericemen- 
tum occur. Redeposit is almost certain unless all morbid conditions 
are removed and extraordinary precautions be taken as regards 
cleanliness, which precautions are difficult to carry out without the 
aid of a dentist. 



Fig. 601 



Fig. 602 






S. S. White scalers. 



Jaquette scalers. (Courtesy J. W. Ivory.) 



Treatment. — The treatment may be divided under three heads: 
removal of deposits, correction of the effects of their presence, and 
prevention of their recurrence. The sole means of removing salivary 
calculi should be instrumental. 

It is frequently recommended that mineral or some of the organic 
acids be used to soften the deposits or facilitate their removal. 
Anyone having seen a case in which a solution of sulphuric acid 
has been used for this purpose needs no further warning against 
the application. Acid solutions will certainly soften the deposits, 
but at the same time inevitably cause a roughening of the enamel 
of the teeth by a solution of the calcium salts. To be sure, the 
acid does affect the calculus more than it affects the enamel, but 
the roughened surfaces of the latter not only invite widespread 
deposits of fermentable material, but render certain the more exten- 



SALIVARY CALCULUS 
Fig. 603 Fig. 004 Fig. 005 



039 



Fig. 606 






No. 3 Scaler. No. 11 Darby- No. 9 Darby-Perry Burton Lee Thorpe' 
Perry scaler. scaler. scalers. 



Fig. 607 



Fig. 008 



Fig. 609 




Pyorrhea scalers Nos. 5 and 
6, revised set. S. S. White 
Dental Mfg. Co.'s Catalogue. 
Intended for use between teeth 
as well as for pyorrhea. 




Flat scaler. 



No. 35 Darby Perry 
excavator. 




C. Kirk's scalers with dentate ends, designed to cut into calculus as 
well as maintain the course of the scaler upon the root side. 



640 



SALIVARY AND SERUMAL CALCULUS 



sive accumulations of calculi in the future. 1 After oral sterilization 
as far as an antiseptic spray or mouth wash will accomplish it the 



Fig. 611 




Crenshaw scalers. (Courtesy J. W. Ivory.) 



1 Recently a proprietary preparation was offered me for removal of stains with 
assurance by the maker that no injurious acid was present. I highly polished the 
labial of an extracted tooth and applied it for one minute. The enamel was dulled 
and roughened. The preparation was acid to litmus. Such preparations sometimes 
are useful in green stain, but should be used with great care and after applied imme- 
diately brushed off with an alkaline powder used as an abrasive. 



SALIVARY CALCULUS 641 

deposits upon the crowns and roots should be removed by means of 
scalers, nearly all used with a draw cut. Dipping the instruments 
in a germicide such as tincture of iodin aids in preventing infection 
of tissue (see asepsis). The instruments should have sharp edges 
and be introduced beneath the deposits, so that the gum be not 
unnecessarily wounded. The scaling should be continued until every 
surface which can be cleaned by these instruments is perfectly smooth. 

For the approximal surfaces of the lower anterior teeth the flat- 
bladed instruments should be used with the push cut, or that in 
Fig. 608 with the draw cut. Younger's pyorrhea scalers are very 
useful (Fig. 623). Thorpe's and Jaquette's scalers are useful. 

For the removal of associated subgingival calculus not too deeply 
placed beneath the gum a No. 35 Darby-Perry excavator is of almost 
universal utility. It is used with the draw cut for the most part. 
A pair of them may be employed and made safe-sided by round- 
ing one edge if desired, to avoid injury of the gum margin. The 
back of the instrument may be sharpened to an edge for a push 
cut. File scalers (Fig. 612) are useful for rubbing off calculus that 





Moose-hide wheels. 

can not be scaled off as a flake. All of the calculi visible, and all 
that can be detected by their roughness, are thoroughly detached 
and scraped away with instruments. The surfaces of the teeth 
are next cleansed with pumice made into a paste with glycerin or 
liquid soap to prevent spattering, and with a few drops of hydrogen 
dioxide for antisepsis; flavoring matter such as liquid Kolynos or 
cologne may be added. The paste is applied to the surfaces of the 
teeth with rubber cups (Young's are excellent), or Abbott's or Rob- 
inson's brush wheels, which are used to cleanse the labial, buccal 
and such lingual faces of the teeth as they will reach (Figs. 614 to 
618). The gum should not be injured. When using brush wheels 
it is well to apply the brush to a point away from the gum and spread 
the bristles against the tooth as it is carried toward the gum. The 
second brush in Fig. 614 is the best for the labial surface and lingual 
of biscuspids and molars, and the third one for the Unguals of lower 
incisors. They may also be used in the angle hand pieces. A finishing 
bur 1 is useful in the removal of thinly distributed hard calculi on lin- 
gual and occlusal surfaces, especially in the mouths of smokers. 

1 Guilford Lectures. 
41 



642 



SALIVARY AND SERUMAL CALCULUS 



The approximal surfaces of the teeth are cleansed with fine linen 
tape or flat floss silk or occasionally with steel or German silver strips 
charged with the pumice paste. More inaccessible parts require the 
hand use of an orange-wood point mounted in a Jack porte-polisher 
(Fig. 619). It is advisable to repeat the polishing with precipitated 
chalk and the same carriers. When prophylaxis is frequent chalk is a 
sufficient abrasive except perhaps with the wood point. 



Fig. 614 




Abbott brush wheels. 



Fig. 615 



Fig. 616 





After cleansing, the associated gingivitis should be reduced and 
the bacteria inhibited while healing by means of an antiseptic 
astringent mouth wash. (See Gingivitis.) 

If desired, the operation may be divided, the gross deposits and 
subgingival calculus being removed at the first sitting. After a few 
days' use of the mouth wash the stains and bacterial plaques upon 
the teeth and any overlooked deposits may be removed. Tincture 
of iodin painted over the teeth brings the deeper stains of the 
collection into prominence, as does also a solution of potassium 
permanganate and both are reasonably antiseptic. 

Register states that a forcible spray of 1 per cent, hydrogen dioxid 
used after the application of tincture of iodin will soften the stains 
and render them more readily removable. The iodin is also rather 
germicidal. 



SALIVARY CALCULUS 



643 



Prophylaxis. — The smoother the surfaces of the teeth are made, 
the longer the redeposition of calculi will be delayed. Black sug- 



Fig. 617 



Fig. 618 



Fig. 619 



T 





gests the use of the ordinary chip syringe and plain 
water, a forcible stream being accurately used to 
wash away the agglutinin. As a means of calculus 
prevention it should be valuable. 

It is a wise measure to cleanse the teeth before 
any long series of operations is undertaken, and 
as a prophylactic measure in the combat with 
caries and pyorrhea alveolaris the operation 
should be frequently performed. Indeed, the 
teeth should be cleansed frequently, so that it 
may not be necessary to remove actual salivary 
calculus, except in those cases in which it col- 
lects with abnormal rapidity. A stick in a metal 
handle for self -prophylaxis is useful if the patient 
will use it. Accurate personal prophylaxis with 
the brush, even a special brush is of great impor- 
tance. (See Prophylaxis.) 

In cases of very rapid recurrence of salivary 
deposits, evidence of an associated sj^stemic 
condition should be sought and, if recognizable, 
should receive appropriate treatment. If not 
recognizable, the method suggested by Black of 
reducing the quantity of food and the thorough 



Jack porte-polisher. 



644 



SALIVARY AND SERUMAL CALCULUS 



mastication of such as is taken, may be conjoined with the occa- 
sional use of Epsom salt, if further needed as suggested. (See page 
633.) A patient treated in this manner by reduction of a heavy meat 
diet to a moderate one with Epsom salt once a week was changed 
during an absence of three months from one whose calculus collection 
seemed enormous from week to week to an amount for the whole 
period about equal to a former week's collection. 



SUBGINGIVAL CALCULUS. 

By subgingival calculus is meant that form of deposit which 
occurs beneath the free gum margin and between it and the tooth. 

Fig. 620 





A, subgingival calculus; B, receding 
pericementum. (Black.) 



Resorption of the septum of bone and 
recession of the gum between the central 
and lateral incisors, caused by deposits of 
serumal calculus under the gingiva?. 
(Black.) 



The deposits consist of small scales or granules, usually quite smooth 
and much darker (olive green) than salivary calculi (Fig. 620). 



Fig. 622 




The alveoli irreparably destroyed by calcic inflammation. (Black.) 



Composition. — They consist mainly of calcium phosphate combined 
with undetermined organic substances. (See pages 630 and 635.) 



SUBGINGIVAL CALCULUS 645 

Cause and Pathology. — It is probable that some degree of marginal 
gum irritation first occurs, though many cases of an apparently 
healthy gum with a scale of calculus beneath it are seen. Whether 
the irritation arises through fermentations about the unclean necks 
of the teeth or as the result of an effort upon the part of the gum 
margin to eliminate calculus as a waste from the system is not abso- 
lutely certain. 

The theory most tenable in view of Black's demonstrations is that 
of calculus deposited by the blood through the gum secretion. 
Bunting imbedded a tooth after moving it about slightly so as to 
create a space, applied saliva and moved the tooth frequently finally 
causing a deposit of calculus along the root. He questioned if 
subgingival deposits in pyorrhea pockets could not come from the 
saliva. 

Effects and Symptoms. — The direct effects are exerted upon the gum 
margin. The gum is either pushed against the crystals or the tooth 
movement pushes the calculus against the gum which is irritated, if 
mildly resorption occurs, exposing the calculus; if more severely 
gingivitis occurs. 

At times the resorption is accompanied by evident marginal inflam- 
mation, at others the gum margin has a normal color, but the resorb- 
ing portion some time is sharply defined by a fine line (or crease) 
from the normal gum tissue, especially at the interdental septum. 
In a more advanced stage this demarked portion appears sunken or 
atrophied, and may have a sort of semihyalin redness characteristic 
of the inflammation. At times the gum margin appears everted 
(Fig. 621 a). If the deposit occur on only one side of a root the 
effects may be confined to that side. 

The lingual root of an upper molar is often exposed for a con- 
siderable portion of its length by successive deposits of calculi. The 
same is true in other situations, notably upon the labial surface of a 
lower incisor. This might be called a form of marginal phagedenic 
gingivitis. 

If the deposit be generally distributed about the neck of the tooth 
the resorption is more equalized. 

In some cases the bifurcation of roots may be exposed and calculi 
deposit in that situation. 

In some cases the gum margin becomes simply atonic or passively 
congested and is pushed away from the teeth by large masses of the 
calculus, which undergo lateral accretion. It appears as a flabby, 
thickened, loosened gum margin, which readily draws about the 
necks of the teeth if the calculus be removed. I have noted this 
in cases of suboxidation with bluish lips, and in renal insufficiency. 



646 



. SALIVARY AND SERUM AL CALCULUS 



Finally, infection may occur about the calculus and the symptoms 
of pyorrhea alveolaris be implanted. When this is established, 



Fig. 623 




9 10 II 12 13 14 15 

Younger's new set of pyorrhea instruments. (Revised by Dr. Robert Good.) 

Fig. 625 




Tompkins' pyorrhea scalers. 



calculi may be deposited farther up the side of the root. This 
pathology often precedes the condition of pyorrhea alveolaris which 
may supervene if pyogenic organisms enter the area. 



HEMATOGENIC CALCULUS 647 

Treatment. — The calculus should be removed by means of delicate 
scalers used with either the push or draw cut, as most convenient, 
after which astringent antiseptic mouth washes should be prescribed. 
The subsequent frequency of removal of causes by oral prophylaxis is 
of great importance. Figs. 623, 624, and 625 show convenient forms 
also useful for the deeper pyorrhea pockets. In most cases healing 
is spontaneous even without medication, but often the washes are 
of advantage. If pyorrhea be present on any tooth it is to be con- 
sidered separately. 

PYOGENIC CALCULUS. 

Pyogenic calculus is that form of serumal calculus which is deposited 
at parts of the tooth root over which pus more or less continually 
flows. Pus, means broken down blood, lymph and tissue which may 
contain calculus derived from the blood as well as may the saliva 
(see page 633). 

In chronic apical abscess the root end may become encrusted with 
it, and in those cases in which apical abscess discharges along the 
pericemental tract it is common to find over the area fine granular 
deposits which vary in color from a light yellow to a reddish brown. 

The same is true of active pyorrhea pockets. 

This calculus prevents the healthy apposition of the gum tissue 
to the roots, probably because of its irritant and infective nature 
(Figs. 513 and 629). 

Treatment. — All such calculi should be removed by whatever 
means possible, which may necessitate scraping the root end or 
its side, or even the amputation of the apical end of the root. In 
some cases 25 per cent, sulphuric acid or Tartasol may dissolve 
it. (See pages 547 and 682.) 

HEMATOGENIC CALCULUS (Syn. SANGUINARY CALCULUS). 

This form of serumal calculus occurs upon the root in the absence 
of apical abscess or a primary pyorrhea alveolaris, and, therefore, at 
points not acted upon by saliva or pus; hence it must be deposited 
by the blood through the lymph, probably as any other form is 
deposited. 

Miller 1 has offered satisfactory evidence of this in a description of 
a case of impacted cuspid well embedded in the bone, and not in 
any way exposed to either saliva or pus influence except that at a 

1 Dental Cosmos, August, 1901. 



648 SALIVARY AND SERUMAL CALCULUS 

point over the cusp the gum underwent suppuration for a short time. 
The crown had undergone resorption, showing local irritation, and 
an olive-green calculus had formed upon the middle third of the 
root. Cases of pericemental abscess have been noted opening 
upon the gum face and presenting dark green calculi upon the root 
in that situation (Fig. 233). (See Pericemental Abscess.) 

Peirce found in such deposits a proportion of sodium urate as 
shown by the murexid test and the cases associated with goutiness 
of the patient. 

While such deposits may not cause immediate irritation, they may 
in time excite inflammation and necrosis of tissue, resulting in a 
discharge of glairy material representative of the condition. This 
form of dental disease will be further discussed as pericemental 
abscess. 



CHAPTER XXI. 
PYORRHEA ALVEOLARIS. 

General Considerations. — In a general way pyorrhea alveolaris may 
be defined as the formation of a progressive gum pocket at the ex- 
pense of the marginal portion of the pericementum, the tooth becom- 
ing progressively loosened. Usually calculi and a pus flow are found, 
but in some cases neither are much in evidence. 

Perhaps it might be advisable to call the cases of pocket with pus 
flow pyorrhea alveolaris and to apply the new term periodontoclasia 
to those cases with pocket but no pus flow. The latter term is hardly 
more applicable to both conditions than the former. Many other 
names have been preferred, but the term pyorrhea alveolaris as 
above defined is the one generally used. 

Apical and lateral abscess from gangrenous pulp or perforation 
are excluded and for present consideration a primary pericemental 
abscess is also excluded. The alveolar wall may be more or less intact 
and rarely either be exposed and necrotic or, as more generally the 
case, be still covered with its internal periosteum, which is the remains 
of the pericementum. In some cases the bone has disappeared by 
resorption and the gum tissue forms the outer covering. Pyorrhea 
alveolaris always involves the consideration of marginal and deeply 
seated gingivitis, but these need not necessarily be pyorrhea. It is 
therefore somewhat difficult to differentiate from gingivitis proper, 
as any form of gingivitis may later assume the characteristics of 
pyorrhea owing to infection (Fig. 634). 

The disease ceases spontaneously with the loss of the teeth, though 
the alveolar process is further resorbed as after any extraction. 

From a prophylactic standpoint it is wise to remove any cause of 
gingivitis as it is apt to lead to a pyorrhea which is usually a disease 
requiring years for its full establishment in a mouth. 

Causes. — It seems that anything which may induce a gingivitis 
may initiate the process when infection is added of a character that 
will destroy the pericementum and produce the pocket at its expense. 

There is much to be said for the theory of Talbot that as individuals 
approach the degenerative period of life, the more transitory struc- 
tures less essential to maintainance of life tend to degeneration, e. g., 
the alveolar process tends to resorptions as particularly noted in 

(649) 



650 



PYORRHEA ALVEOLARIS 



general marginal resorption of gum and bone. (For further details, 
see p. 625.) 

This condition of presenility, while claimed to be a forerunner of 
general pyorrhea by Talbot, Hopewell-Smith, Hecker, Roy, Cazier 
and others, is not claimed to cause pyorrhea by itself, but to act as a 
predisponent to local infections and a complication when it is estab- 
lished. This is also much confused by the fact that so many causes 
of local irritation of mechanical nature with their consequent inflam- 
mation of gum margin or pericemental inflammation (with resorption 
of bone), and by constant uncleanliness and probable infection of the 
gingival tissues that in most cases it can only be a surmise. The fact 

Fig. 626 




y 




Endameba buccalis. Illustrating nuclei, ingested matter and bacteria, also at A and 
B the ectoplasm and ectosarc. Half second intervals. (Price.) 



that pyorrhea usually occurs after thirty years of age in some degree 
bears this theory out, but again other causes have gradually accumu- 
lated. Hopewell-Smith 1 considers the constant infection of the gingival 
trough a predisponent of the degeneration. Any of the causes which 
produce chronic non-septic pericementitis (see page 589), may produce 
an inflammatory degeneration which will produce looseness, mal- 
occlusion, etc., tending to mechanically increase the inflammation. 
This is generally recognized as a cause of pyorrhea in that it predis- 
poses to the development of bacteria already in the gingival trough. 
The pyorrhea produces more looseness so that a vicious circle is 



L 



1 Dental Cosmos, 1918, p. 428. 



GENERAL CONSIDERATIONS 



651 



established. The narrowness of the neeks of teeth (in conjunction 
with length of crowns at times) is also a predisponent to infection 
in that bacterial collections are more readily formed, or calculus and 
food deposited. Again this cause is aggravated and malocclusion 
introduced when teeth tilt in consequence of extraction. Mechanical 
irritants such as crowm margins, calculus beneath the gum margin, 
also institute an inflammation favorable to bacterial action. 

The Infective Element. — Much work has been done to determine the 
primary infective cause of pyorrhea. 

The present thought is that pus formation is a secondary effect 
implanted upon a primary infection of non-pyogenic character. That 

Fig. 627 




Endameba Kartulisi. Showing organism starting on a journey and its progress 
in six seconds. Half second intervals. (Price.) 



is, that mainly the pyogenic bacteria enter a prepared field. Regard- 
ing this primary infection two views are mainly discussed: 

1. That the cause lies in oral endamebse. 

2. That bacteria are the causes. 

1. In 1914 Smith and Barrett 1 announced their belief that endameba 
gingivalis (Gros) was a protozoal cause of pyorrhea alveolaris. It 
also has the name Endameba buccalis. In a paper written in 1915 2 
They reaffirm their belief, having then accumulated 325 cases and 
demonstrated their presence in 318 of these. They do not claim that 
all cases are due to them, but recognize spirochetes and other bacteria 

1 Dental Cosmos, August, 1914. 

2 Dental Items of Interest. 



652 PYORRHEA ALVEOLARIS 

as possible causes of a reasonably small number of cases. Chiavaro 1 
also found them in 1914, but regarded them as harmless commensals. 

Bass and Johns 2 claim to have found them in the depths of care- 
fully examined pockets in nearly all of several hundred cases of pyor- 
rhea "disappearing as the lesions get well." This finding in all cases 
has not generally been confirmed. 

Smith and Barrett and Bass and Johns state them not present in 
really normal gums while Park and Williams 3 state that they are 
found in the mouths of a majority of children without definite rela- 
tion with the beginning of pyorrhea. As pointed out by Smith and 
Barrett this is merely a prevalence of cause not a proof of non- 
pathogenicity. Bass and Johns claim that endamebse engulf bacteria 
and carry them into deeper parts of the pockets, to there develop. 

Smith and Barrett argue for a possible symbiotic relationship 
between endamebse and bacteria, i. e., the action of bacteria is 
implanted upon a field prepared by the endamebse, while others 
argue that as the endameba? phagocyte large numbers of bacteria 
they are commensals and mere scavengers or even beneficial. 4 Hart- 
zell and Henrici were unable to find them in the living ulcerated tissue 
forming the border of pyorrhetic pockets, but Price found a Kartulisi 
in such, tissue. 

Price 5 found endamebse in cases after treatment with emetin when 
none could be found before or during treatment of some cases. 

Endameba kartulisi is also found and occasionally those of the 
Endameba coli type. 6 Endamebse are uncultivable in media and 
Koch's postulates are considered at present impossible of fulfil- 
ment. Smith and Barrett have kept them alive seventy-two hours 
in solution of egg white. The basis upon which these claims rest is 
their common presence in the lesions and their vulnerability to dilute 
solutions of emetin 1 to 100,000 or less which is not also germicidal 
(the usual 0.5 per cent, being so) and their vulnerability to emetin 
hypodermically or alcresta ipecac internally (see therapeutics) which 
when reaching the pericementi is at least 1 to 200,000 dilution. Keyes 7 
followed Barrett's technic with success. Rhein 8 (also Kells 5 ), cured 
a case with it when other treatment failed and the author has had 
occasional success in obstinate cases otherwise treated. There is a 

1 Dental Cosmos, September, 1914. 2 Text Book Alveolo Dental Pyorrhea. 

3 Text Book Pathogenic Microorganisms, p. 531. 

4 See Hartzell and Henrici: Journal of National Dental Association, 1915, p. 128, 
for elaborate arguments to this effect. 

6 His splendid series of arguments for and against the causal relation of endamebae 
may be found in the Journal of the National Dental Association, May, 1915. 
6 Ibid., p. 23. 7 Dental Cosmos, 

s Dental Items of Interest, December, 1916, p. 883. 



GENERAL CONSIDERATIONS 653 

tendency to abandon the theory, but to the writer it still seems pos- 
sible while no other is proved absolutely. Two forms of technic have 
been suggested for microscopic examination. 

Smith and Barrett take the purulent contents from the bottom 
of the pocket, diffuse this in a drop of slightly warmed saline solution 
on a warmed slide and immediately examine it while living with a 4 
mm. lens. (Bass and Johns suggest the use of 5 or 6 times the quan- 
tity of saliva as keeping them alive a longer time.) They describe it 
as having active ameboid movements for about fifteen minutes, but 
eventually becoming quiescent. They vary in size from 6 or 8 mi. to 
30 mi. in diameter. They have a clear ectosarc which extends when 
pseudopods form and a coarsely granular endosarc which extends 
but slightly and contains numerous food vacuoles containing frag- 
ments of leukocytic chromatin and apparently portions of red blood 
cells. No contractile vacuole exists. Motile and non-motile bacteria, 
epithelial scales, leukocytes, etc., are present in the microscopic 
field. 

Smith and Barrett suggest the following method of staining: 

1. Fix in warm saturated solution of bichlorid of mercury in 
alcohol. 

2. Stain with Giemsa's stain. 

Bass and Johns 1 stain them by the following technic : 

1. The material from the bottom of a pocket is spread thinly on 
a microscopic slide and fixed carefully by heat. 

2. This is then covered with one or two drops of carbol-fuchsin 
and then washed off at once with water. 

3. One or two drops of Loffier's methylene-blue solution is applied 
for fifteen to thirty seconds. 

4. This is then washed off with water and dried with a blotter or 
by fanning in the air for a few minutes. When properly stained the 
film appears purple to the eye. It should not be over stained with 
methylene blue as this displaces the red stain. At the right point, 
sharp contrasts of value occur. 

The examination is made with an oil immersion lens. The following 
differentiations in the field are noted by Bass and Johns. 

Staining Pink. — Some bacteria, red blood cells (also in the enda- 
mceba), cytoplasm of pus cells (leukocyte), cytoplasm of epithelial 
cells, ectosarc of endamcebse (sometimes light purple), nucleus of 
endamcebse. 

Staining Purple. — Some bacteria as spirochetes, nuclei of pus cells 
(leukocytes), nuclei of epithelial cells, cytoplasm of some large cells 

1 Text Book, Alveolo-Pental Pyorrhea, 



654 PYORRHEA ALVEOLARIS 

from granulating surfaces, ectosarc of endamoeba, at times a light 
purple, endosarc of endamoeba?. 

Stai?u7ig Blue. — Some bacteria, sometimes endosarc of endamoeba?. 

2. Opposed to the amoebic theory is that of Hartzell and Henrici 1 
for streptococci, Noguchi for spirochetes or treponemata and Medalia 
and others for mixed bacterial infections. Hartzell and Henrici, from 
numerous observations, state that the gingival crevice is always open 
and subject to infection from tooth surfaces and saliva (see page 650) . 
That the veins and perivascular lymph spaces can carry infection from 
the gingival crevice to the peridental membrane (and socket apex), 
which movement of infectious material is aided by the enormous 
force of mastication. That when proper care to exclude extraneous 
infection is used the peridental tissues alicays produce grouih of 
Streptococcus viridans. In another article, they consider pyorrhea 
primarily a granulomatous growth analogous to apical granuloma 
(primarily non-purulent). Hopewell-Smith 2 adds Micrococcus ca- 
tarrhalis and mentions epithelial debris, phagocytes, together with 
countless bacteria as a normal state of the gingival trough. 

Hartzell and Henrici further state 3 that oxygen can be blown under 
compression into the gingival crevice and into the tissues evidencing 
"physical imperfections" (probably normal spaces) (see Emphy- 
sema, page 504). Later other pyogenic bacteria enter and produce 
pus. Spirochetal forms of bacteria are frequently found in the 
pockets, notably the following: 

" A large spirochete with wide curves in its spiral, morphologically 
greatly resembling the spirochete of recurrent (relapsing) fever 
(Kolle 4 ). Treponema mucosum producing the odor of pyorrhea in 
its medium (Noguchi). 5 

The use of salvarsan both locally and systemically is antagonistic 
to them, hence by therapeutic test they are claimed as a cause by 
(Kritchevsky and Seguin 4 ). It may be that such success as is 
achieved by succinamide of mercury hypodermically administered is 
to be regarded as also some like evidence as they disappear after the 
treatment. The spirochetal forms remain after endamoeba? disappear 
and are subject to iodin locally applied or any one of the arsenical 
group as neosalvarsan or arsenobenzol 6 (Smith and Barrett). 
Kritchevsky and Seguin have ably illuminated this view (page 690). 

1 Conveniently found in Dental Items of Interest, December, 1916, p. 932, also see 
Journal of National Dental Association, May, 1917, p. 123. 

2 Journal of National Dental Association, May, 1917, p. 492. 

3 Dental Cosmos, May, 1918, p. 428. 

4 Dental Cosmos, 1918, p. 781. 5 Journal of Experimental Medicine, 1912, p. 194. 
6 Dental Review, October, 1915. 



GENERAL CONSIDERATIONS 655 

They used neosalvarsan intravenously and succinamide of mercury 
intramuscularly in cases of marked pyorrhea with and without local 
treatment and effected almost complete disappearance of spirochetes, 
claiming that only the rarer and inactive forms remain. They also 
confirm Smith and Barrett in their claim of value for neosalvarsan 
used in the pockets. They advise also local surgical treatment and 
subsequent prophylaxis, not claiming any establishment of immunity 
from recurrence, also that much loosened teeth should be extracted. 
(See Treatment.) 

Medalia, in 1913, 1 before these demonstrations made scientific 
studies of the bacteria found in mild and advanced cases together 
with those found in the feces of the same patient and compared the 
finding with the opsonic index of the patient to the prevailing bacteria. 
In 112 cases he found by direct examination of smears and cultural 
findings the following important bacteria. 

Bacteria. 

Times. 

Pneumococcus (in chains or diplococcus forms) 26 

Pneumococcus and staphylococcus together 67 

Pneumococcus and streptococcus together 3 

Pneumococcus, streptococcus and staphylococcus 10 

Pneumococcus and Micrococcus catarrhalis 1 

Staphylococcus and Micrococcus catarrhalis 2 

Staphylococcus aureus 2 

Staphylococcus and streptococcus 1 

Sterile 3 

In 85 advanced cases the cultural findings were practically in the 
same proportion. The opsonic index of 49 of the patients was as 
follows. 

Bacteria. 
Pneumococcus . 
Staphylococcus 
Streptococcus . 
Colon (B. coli) 

These patients treated by appropriate vaccines made marked 
improvement when local treatment was conjoined, the results in 
the incipient and moderately advanced cases being almost perfect 
while in advanced cases out of 85, 37 were reported cured, 40 bene- 
fited, 4 unimproved, 3 dropped out of treatment. These findings 
seem to show at least that the above bacteria are at least strongly 
complicating factors in at least maintaining a pyorrhea. 

The present view of bacteriologists that the Streptococcus viridans 
may assume both a streptococcal and pneumococcal form (diplo- 

1 Dental Cosmos, 1913, p. 24; 150, 704, 



Below 


Above 




Not 




normal. 


normal 


Normal. 


tested. 


Total. 


39 


2 


7 


1 


49 


25 


1 


20 


3 


49 


4 


— 


32 


13 


49 


18 


3 


12 


16 


49 



656 PYORRHEA ALVEOLARIS 

coccus) tends to harmonize the views of Medalia, and Hartzell and 
Henri ci. 

These demonstrations while rendering the subject of bacterial 
infection clearer have not finally disposed of the problems as to 
whether the Streptococcus viridans, etc., acts as a direct cause or 
awaits the primary action of calculus, etc. 

There are two views regarding the calculus found in pyorrhea cases : 

1. That it is primarily deposited under the gum margin (see theories 
of Black, Bunting, etc., page 632), and becomes an irritant, causes 
inflammation mechanically and this favors further action by bacteria. 

2. That infection occurs, irritates tissue, causes abnormal secretion 
in which the elements of calculus are contained which combine and 
precipitate as calculus or the calcospherites of calculus are thrown 
out in the secretion as in the saliva (see page 632) and deposit on 
the tooth neck. 

In either case calculus formation is an early stage in the production 
of pyorrhea. 

That there are some cases in which the infection and inflammation 
precede any clinically evident calculus formation is a known fact 
as shown by a bright red, acutely infected gum margin. This when 
treated early by mechanically cleansing and chemically disinfecting, 
the part is at least temporarily cured. It is usually noted in mouths 
in which a more advanced infection may elsewhere be found. 

Granting the fairly established fact of the common infection of the 
gingival trough before any appearance of calculus and the gradual 
accumulation of infection and calculus through a series of months or 
years and the usual cure when cleanliness is established, it is rational 
to assume that the second theory above described is at least a work- 
ing theory upon which prophylaxis and cure may be based until the 
actual facts shall be proved. Therefore in observing mouths at all 
times one should look ahead for all forms of gingivitis or causes 
liable to produce it to a possible future pyorrhea and take measures 
to prevent it (see page 650). 

Clinically, fully established cases of pyorrhea alveolaris may be 
divided into three classes: (1) Cases associated with a primary 
gingivitis and with the formation of hard, scaly, dark, annular 
calculi beneath the gum margin (subgingival calculus), the pockets 
not usually extending far beyond the deposits; (2) cases beginning 
with a marginal gingivitis and apparently not dependent upon the 
association with calculus, though frequently complicated by it; 
(3) cases having an apparent origin at some point between the 
gingival margin and the apical tissue, the gingival margin at first 
being apparently intact. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 657 

It is probable that the infecting agents in these types differ in 
their nature, or that in the event that they may be proved to have 
a similar origin the tissues react differently to them, either partially 
resisting them, forming calculus as a result of the irritation, or 
rapidly giving way to them, permitting a deep action. In this con- 
nection it is probably better that each case be microscopically con- 
sidered and the local medicinal or systemic treatment be conducted 
in accord with the findings and the clinical expressions. 

In the abscence of known causes the conditions may be divided 
according to their clinical expressions. 

In the consideration a pus flow due to apical abscess, lateral abscess 
upon a perforation, or that due to obvious salivary calculus (for 
these, see under proper headings), also simple gingivitis or deeply 
seated gingivitis, not resulting in the clinical feature of pyorrhea as 
defined, are excluded. 

PYORRHEA AVEOLARIS BEGINNING AS A MARGINAL GINGI- 
VITIS AND ASSOCIATED WITH SUBGINGIVAL CALCULJJS. 

Causes. — The causes of this condition are those predisposing and 
exciting causes of marginal gingivitis which have been described. 
(See page 607.) Several local factors have to be considered in this 
connection: (1) The marginal infection; (2) the irritative effects of 
any calculus that may be formed; (3) the deep infection by pyogenic 
organisms; (4) the modification of the progress of the disease by the 
attendant loosening of the teeth and death of the pulp. 

Fig. 628 




Case of a boy, aged fourteen years, with pyorrhea, especially on lower anteriors, 
with hypertrophic gingivitis. 



Clinical History, Pathology, and Symptoms. — There is usually an 
unclean condition of the teeth; infection exists either in tenacious 
films of bacteria attached to the necks of the teeth and requiring 
iodin disclosing solution for their detection, or in masses of detritus 
readily noticeable. Subgingival calculus is, as a rule, obviously 
present (Fig. 633). 
42 



(358 



PYORRHEA ALVEOLARIS 



The gum margin may be atrophied or be inflamed; or it may have 
a fairly normal appearance. When the gum margin is pressed upon, 
pus may be squeezed out in variable quantity; even when not apparent 
there may be an exudate containing pus corpuscles. 

It is assumed that the local infection brings about the deposit of 
mucous exudates rich in calculus (see page 632, for origin), at a point 
beneath the gum margin, and that formation of subgingival calculus 
occurs, followed by pyogenic infection and pus formation. 

The gum may now be resorbed either w.ith apparently normal 
bulk or the margin may be everted and thickened into a cord-like 

Fig. 629 




Serumal calculus, showing stalactite-like formations. (Talbot.) 



margin which is either of normal color or inflamed, sometimes there is 
no apparent change in the gum margin or it may be thin and pale; 
the absorption of the gum causes the exposure of the calculus (Fig. 
620). In this manner the bifurcations of the roots may be uncovered 
and calculi be deposited in that situation. The resorption may only 
be confined to one side of a root and be the result of several successive 
depositions which may remain when the gum recedes, or which may 
be removed and again be deposited. In this way the side of the root 
may be exposed nearly to, and in some cases quite to, the apex. 
The destruction of the tissues may assume several forms. In 
certain mouths, especially in neurasthenic and anemic patients, a 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 659 

viscous material may accumulate upon the necks of teeth or exposed 
roots; and the pericementum, bone, and gum may rapidly inflame 
and disappear, leaving the roots exposed to collect more of the 
material, while pus may not be much in evidence. 

Fig. 630 




Destruction of pericementum, bone, and gum over buccal root of a molar. 
(See also Fig. 583.) 

The resorption may occur as shown in Fig. 631, or the gum may 
be split and the destruction follow the length of the root on one side 
only until even the apex is reached (Fig. 630). 

The tooth may be loose or firmly attached by the remainder of the 
pericementum. This is especially true of those teeth having very 
narrow necks, in which the roots describe a prominent curve just 
above the cervix. 

Fig. 631 




Resorption of gum over palatal root of an upper molar, associated with but trifling 
deposit of calculus, but the root is covered with a viscid deposit. Aged thirty-two 
years. Patient neurasthenic and of tuberculous diathesis. Condition in 1904. Tooth 
lost in 1907. In 1912 several other teeth were lost. In 1914 several more had gone. 
In 1918 the last upper six anteriors removed. 



In such cases the pus pocket may not be deep and the pus formed 
may readily be washed away. Such cases present some resemblance 
to simple gingivitis and might be so classed or as periodontoclasia 
if there were no pus flow. Instead of this the pericementum may be 
progressively destroyed by suppuration and the gum margin remain 
practically intact. In these cases the pus flow is more abundant, a 



6G0 



PYORRHEA ALVEOLARIS 



deep pocket is formed, extending a third or even two-thirds or more 
of the length of the root (Fig. 622). It is common to find beads 
of calculus deposited along the side of the root and presumably of 
serum al origin. The cementum being deprived of nutrition, its 
minute nutritional openings or openings containing fibers harbor 
bacteria or the shreds of necrotic infected pericementum may remain 
on the root surface. 

These inflammatory disturbances necessarily involve deeply 
seated gingivitis or infiltration of leukocytes into the interstitial 
connective tissue of the gum. As pointed out by Talbot, resorption 
of various kinds and at times constructive changes accompany such 
an inflammation. (See Deeply Seated Gingivitis.) Endarteritis is 
also noted. All varieties of degeneration of the remaining -tissues are 
noted in advance of its further progress. « In the early stages of the 



Fig. 632 



Fig. 633 




Pyorrhea pockets. Mesial root of 
molar largely denuded. Treated by 
amputation. ("Price. ) 




Section of an upper incisor, showing at 
a, a, a deposit of serumal calculus within 
the free margin of the gum. (Black.) 



disease the probe usually fails to discover uncovered alveolar bone, 
although it may rarely do so. If not uncovered its loss is due to 
resorption; if, however, necrotic and bare alveolar bone be found, it 
is undergoing a molecular necrosis under the influence of the pyogenic 
organisms. 

In some cases the pericementum may be destroyed at the cervical 
third of the root, the alveolar process may be resorbed on its inner 
surface, and an accompanying constructive irritation may cause 
the deposition of bone upon the outer aspect of the alveolar process; 
the gum margin is also thickened by cell proliferation. The con- 
dition imparts the appearance of hypertrophy of the gum and gum 
margin (Fig. 634). The gum may recede from this position and expose 
the calculus yet remain puffy and cord-like and even ragged forming 
a convenient nidus for food, mucus, etc., which gives the part an 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 661 

angry, slimy look. The inflammation of the pericementum may 

become general and the attendant swelling forces the tooth into 
malocclusion with its antagonist. The mechanical factor is now 
introduced and the extrusion increases gradually or even rapidly. 
Even if not very much extruded looseness due to inflammation and 
bone resorption begins. Sometimes such teeth can be ground one- 
eighth inch before removing the excess occlusion. Such constant 
pounding is deadly. By placing the ringer over the tooth and direct- 
ing closure of the jaw this malocclusion will be noted to cause "buck- 
ling" or forcing of the teeth to one side. 

When about one-half or more of the root has been stripped of 
pericementum and deprived of alveolar support, looseness and 
extrusion of the tooth become marked. 



Fig. 634 



Fig. 635 




Section of an upper incisor, showing 
destruction of the peridental membrane 
and eversion of the alveolar wall, with 
thickening of its border: a, serumal cal- 
culus; b, thickened border of the alveolar 
wall; c, pus cavity. (Black.) 




Section of an upper molar with its 
alveolus, etc., showing deposit of serumal 
calculus under the gingival borders: a, a, 
serumal calculus. (Black.) 



The advance of the disease now becomes more rapid; the undue 
mobility and malocclusion of the tooth excite an inflammatory 
reaction beyond the directly infected part; so that soreness and 
looseness are further increased. Extraction at the later stages 
reveals a thickened apical pericementum as the sole attachment to 
the bone. After the looseness of the tooth becomes marked, the 
pulp of the tooth undergoes hyperemic changes, reacts to thermal 
stimuli, and often dies. Pulp nodules often are formed before its 
death. Reflex symptoms may occur at this stage when the pus 
pocket approaches the apex. Hartzell and Henrici claim that the pulp 
may be infected before the pocket reaches the apex. (See Pulpitis.) 
Infection of the dead or practically dead pulp 'readily occurs via 



662 PYORRHEA ALVEOLARIS 

the pocket (sec Fig. 630), and apical suppuration arises. The 
symptoms of the latter condition are modified, according to the 
facility with which the pus finds vent along the pyorrhea pocket. 
(A true apical abscess or aggravated pyorrhea resulting.) In some 
cases pericemental abscess becomes associated before the apical 
tissues are involved. The disease proceeds until the affected tooth 
or teeth are cast out, the alveolar walls having been largely absorbed, 
and the pericementum largely destroyed. The remainder of it is 
usually swollen. The disease ceases with the loss of the affected teeth, 
leaving a flattened or absent alveolar ridge covered by a mass of more 
or less spongy gum tissue, though some cases of necrotic alveolus 
occur. 

The duration of this disease may be months or years, and a number 
of teeth may be affected at once. A general subcatarrhal condition 
of the mouth usually attends the disease. The presence of pus 
often imparts to the breath a peculiar, sweetishly fetid odor which 
may, however, be masked by an odor of putrefaction (pigsty or 
sewer-gas odor). Nasal catarrh may also be present whether as a 
cause or effect is not proved, but it may nevertheless be a continuing 
cause unless relieved. 

It is often the case that the shifting of pyorrhetic teeth due to 
swelling of the pericementum permits them and the other teeth to 
move into a position in which they malocclude. This brings in a 
mechanical cause of interstitial gingivitis, which, with the existing 
infection, brings other teeth into the pyorrhetic state. 

Diagnosis. — When a probe can be passed for an undue distance 
into the gingival space and along the root it is well to consider the 
case one of pyorrhea whether pus is evident or not and to institute 
treatment. 

Radiographic examination will frequently show x apparent areas of 
rarefaction which are not always pockets as deep as shown, but often 
associated with the beginnings of the disease. Fig. 637 shows a case 
of a slightly loose left upper lateral in which the pocket would seem 
to extend nearly to the apex but could not be explored so deeply. 
Fig. 569 shows a somewhat loose bicuspid supporting a bridge and 
overworked. The condition is the same, resorption of bone, but no 
actual|pocket.( 

^The nature of the infection. can only be determined by a micro- 
scopical examination (see page 653). 

Associated Abscess. — In a number of cases of deep pyorrhea pockets 
an infection of the aveolar structure, or, at least, of the tissue remain- 
ing over the deepest portion of the pocket, may occur, and an abscess 
form which discharges by a fistula through the labial or lingual 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 663 

aspect of the gum. It is to be regarded as an abscess secondary 
to a primary pyorrhea alveolaris. The passage of a silver probe 

* Fig. 636 




Inflammation of pericementum, endarteritis obliterans. Talbot's case. (Latham.) 

through the two sinuses at once will reveal this (Fig. 638). In a 
tooth treated for apical abscess such a pyorrhea pocket existed, and 

Fig. 637 




Left upper lateral firm, but radiograph shows bone resorption. A pocket could 
only be found on the distal for about half the apparent distance. Practically no pus. 
This patient, however, developed a pericemental abscess at the depth of a pocket 
on the right upper second bicuspid, which I cured by instrumentation. 



doubt arose as to the cause. The fact that it was near the gum 
margin and the probe could not be passed into a sinus leading to a 



664 



PYORRHEA ALVEOLARIS 



root-end was considered evidence of abscess secondary to pyorrhea. 
Evacuation and antisepsis were sufficient to effect a cure. 

In one case of pyorrhea alveolaris of the variety under considera- 
tion the pocket existed upon the mesobuccal aspect of a right lower 
third molar. The second and first molars were absent. The pus 
dissected away the periosteum of the bone and formed a large abscess 
over the entire area of bone between the third molar and second 
bicuspid. After evacuation of the abscess, the probe was passed 
through it to the pyorrhea pocket (Fig. 639). A still simpler form than 
that shown in Fig. 638 has occasionally occurred. The pyogenic 
organisms have burrowed from a gingival space normal in extent 
into the tissue of the free gingival margin forming a true marginal 
abscess. Another expression occasionally occurs. The infection 
travels via the natural channels in the pericementum from the pyor- 



Fiq. 638 



Fig 639 





Gingival abscess secondary to pyorrhea 
alveolaris: C\ calculus in pyorrhea pocket; 
F, fistula leading to pocket PP; B, bone 
on lingual side. 



Diagram of abscess secondary to pyor- 
rhea alveolaris (see text) ; PP, pyorrhea 
pocket; AC, cavity of secondary abscess; 
B, bone. 



rhea pocket to a deeper point in the pericementum (for example, to 
a point one-quarter inch or more below) producing what is called a 
pericemental abscess (see page 698). The tissue between may seem 
unbroken and the fistula may seem like that associated with chronic 
apical abscess. Fig. 640 will illustrate the manner in which this may 
occur. In a case of a pyorrhea pocket on a lower lateral, transillu- 
mination showed a bright red spot at a point a quarter-inch below 
the pocket, and to the side of the root. The pain was intense, and 
only relieved by opening at this point with a lancet. In another 
case a fistula appeared on the buccal gum about one-third inch above 
the margin and between the buccal roots of an upper molar. The 
crown was tapped by a student for dead pulp, but exposure of the 
pulp demonstrated its vitality. Exploration showed a distolingual 
pyorrhea pocket leading into the bifurcation between the distobuccal 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 665 

and lingual roots. From thence the pericemental abscess discharged 
buccally between the buccal roots. 

While dental caries may occur with pyorrhea alveolaris, it is usual 
to find the teeth of the most highly organized structure. The pulp 
tissue is usually increased in density, and there is a tendency to 
the constructive changes, secondary dentin, nodules, etc., and the 
inevitable degenerative changes following these diseases. This may 

Fig. 640 



. * r M^^. 


» j 


siiiftfte 


V 


■ % 






■■■■•• 



Pericemental abscess associated with a pyorrhea pocket. (V. A. Latham.) 



be due to tooth movement which causes pulp stimulation or may at 
times be due to the gum recession which exposes the cement uni. 
This wearing away, the dentin is exposed, fibrils are irritated and con- 
structive changes by the pulp result in secondary dentin or nodules 
or both (see pages 359 and 367). Hypersensitivity of necks is also 
found in some. - 
It has been contended that these pulps are responsible in a measure 



666 PYORRHEA ALVEOLARIS 

for the pyorrhetic condition, but it is now regarded as not only 
unlikely, but that the teeth with vital pulps are most amenable to 
treatment. The contrary process is more than probable, as pyorrhea 
frequently causes a pulp hyperemia which subsides with the cure of 
the pocket. (See Deeply Seated Gingivitis.) 

Prophylaxis. — As outlined above, the prevention of pyorrhea 
alveolaris of the first class involves the removal of the local and, if 
possible, the systemic causes of the gingivitis, if any exists, and the 
systematic cleansing of the teeth at short intervals. The daily use 
of the tooth-brush and antiseptic powders and washes by the patient 
is also important. 

D. D. Smith advises, for this class of cases, a thorough cleansing 
once a month, or at first even oftener. The cleansing is to be done 
with an orange-wood point, grasped in a Jack porte-polisher and 
charged with pumice paste, best made with hydrogen dioxid, or water 
containing tincture of iodin or iodoglycerol. The local sources of 
gum infection are thus continually removed and the gums stimulated 
by the mechanical irritation with the wood point. Bridges require 
careful cleansing. (See Prophylaxis.) 

Treatment. — The treatment of well-established pyorrhea alveolaris 
of the first class is to be considered under three headings: (1) The 
removal of pus, calculus, and bacterial films; (2) the prevention of 
extreme mobility; (3) the medicinal treatment local and general, the 
prophylaxis, or prevention of a relapse into the diseased condition. 

The Removal of the Local Causes. — Calculus and the always 
associated infection being an obvious irritant, they should be removed 
from crowns and all parts of the roots. To prevent infection of sur- 
rounding tissues and to remove the pus present the pockets are to 
be flushed out with hydrogen dioxid, which may be done by means 
of a syringe with fine nozzle after spraying out the superficial parts 
by means of an atomizer operated by compressed air. The forcible 
spray lifts away the gum margin and cleanses mechanically as well 
as chemically though not the depths of the pockets. The mouth is 
reasonably cleansed at the same time. Also the use of Talbot's 
iodoglycerol full or quarter strength is a good preliminary germicidal 
treatment. If large quantities of supragingival calculus exist, it is 
well to next remove the gross deposits and permit the patient to use 
an astringent, antiseptic mouth wash for a few T days, or the operation 
may be proceeded with, using trichlorid of iodin, 1 to 1000, as a 
germicidal wash. 

Free bleeding is beneficial to the inflamed tissue. The removal is 
accomplished with scalers of any suitable form, working either with 
push or pull cut as best suits the case, the latter being much less 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 607 

painful, as a rule. As a further preventive of infection the writer 
uses tincture of iodin or Talbot's iodoglycerol picked up on the 
scaler by dipping it in a portion in a minim glass. Waas 1 uses as a 
result of bacterial test a 1 per cent, solution of iodin trichlorid. He 
found it to kill cocci in fifteen seconds. It may be injected into the 
pocket. For the purpose of disinfecting instruments in passing from 
pocket to pocket he wipes off the debris, passes it a few times through 
a 5 per cent, solution of mercuric oxycyanid, washes in ethyl alcohol 
and burns off the latter. The alcohol and burning off alone is 
commended by Medalia. 

Fig. 641 illustrates the method of guarding against unnecessarily 
wounding the soft tissues. If the calculi be extraordinarily inacces- 
sible the pockets may be enlarged by packing for ten or fifteen min- 
utes with cotton tampons saturated with the 10 per cent, trichlor- 
acetic acid, which also softens the calculi, or salicylized cotton may 
be left in the pocket for a day (Black) or cotton may be packed into 
a deep pocket and soaked with 20 per cent, aqueous solution of 
hydrogen ammonium fluorid plus 10 per cent, free hydrochloric acid 
(see page 682). In some cases novocain injections or applications of 
powdered cocain carried into the pocket on the working instruments 
must be made to prevent excessive pain, or a mucous or conductive 
anesthesia may be resorted to, the teeth under its influence being 
thoroughly scaled and any surgical work on the gums done. After 
removal of the bulk of calculus with scalers any fine granules gummy 
collections or shreds of pericementum should be well rubbed off 
with Rhein's approximal trimmers, or Smith's pyorrhea instruments, 
or the scalers. This removes the bacterial plaques as well. After 
this medicinal applications are made (see later). The scaling of 
each tooth is to be completed at one sitting, as repeated scalings 
interfere with the regenerative process, and the pocket is most 
accessible at that time, and, as a rule, one thorough scaling is far 
better than a number of incomplete ones. Several teeth may, how- 
ever, be done (note on page 684, Barrett's method as an exception). 
In cases with deep pockets it is advisable to treat only a few teeth, 
both because of the necessary infection, but also because much 
general inoculation may result and might cause metastatic infection. 
Hartzell claims that if the cemental surface be scraped away to the 
depth of the attachment of the peridental fibers a source of infection 
lying in these minute openings will be removed, and the surface will 
be left smooth. 2 The lacunas of the cementum should not be invaded. 
Barrett has shown that the thinnest possible histological preparation 

1 DeDtal Items of Interest, March, 1918, p. 168. 

2 Dental Cosmos, 1908. 



66S 



PYORRHEA ALVEOLARIS 
Fig. 041 




Showing the manner of holding an instrument for detaching calcareous deposits 
when using the pushing motion. The third finger rests on the edges of the teeth, allow- 
ing freedom of the hand to make rapid and effectual movements in dislodging the 
calculi. 



Fig. 642 



Fig. 643 





Scalers (three times natural size). 



Illustration of the position and form oi 
incision through the gum for exposing the 
root of the tooth and injured alveolar pro- 
cess: a, incision. (Black.) 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 669 

of cementum ground from the pulpal side only shows lacunae present, 
so that it is probable that some will be invaded, at least one cannot 
say they are not in a practical case* (Fig. 645.) 



Fig. 


644 




^" 


*? 


^ 


11 


a 


J 



Persistent flow of pus from their gum margin. Promptly checked and case cured by 

gum removal. 

The gum margins are not to be unnecessarily wounded, but very 
redundant granulations may be cut away, and sometimes a soft, thin 
gum margin which persistently does not become attached, but holds 
pus bacteria, should be cut away to the bone margin, or removed 
with a cautery. Gentle curettement of these soft tissues will excite 



Fig. 645 




Section of cementum ground from the pulpal side only, showing numerous lacunae. 

(M. T. Barrett.) 

free bleeding and stimulate granulations, both being desirable. In case 
the pockets are so deep or have such form that the scaling cannot be 
done without overstretching or injuring the gingival edges, Black ad- 
vises that gum flaps be raised, exposing the alveolar margins (Fig. 643) . 
A semicircular incision is made and turned back, and bleeding checked. 
By means of sharp chisels the alveolar borders are freely scraped, the 



670 PYORRHEA ALVEOLARIS 

pockets are flushed with hydrogen dioxid, and the flap secured by a 
couple of stitches (a pad of cottonoid wet with a mild antiseptic placed 
over it serves as well). Local anesthesia should precede this opera- 
tion. The same writer advises, in cases where eversion of the alveolar 
margin has occurred, that the process be exposed by cuts and broken 
down by three cuts made with a sharp chisel and mallet; the loosened 
segment of bone to be pressed firmly against the root. It is desired 
next that the entire pocket will fill with granulation tissue, and organi- 
zation of the granulations take place, furnishing reattachment. That 
this occurs in some cases is undoubted. A good clot is the best 
occupant of the space. A reproduction of alveolar margins also 
occurs in some cases. The hope of good results lies in keeping the 
parts reasonably aseptic after all foreign deposits and dead material 

Fig. 646 Fig. 647 





Pyorrhea pocket in bifurcation. The same treated by scraping and filling 

with gutta-percha or oxyphosphate of cop- 
per. (Radiographs by Price.) 



have been removed. An exposed pocket in the bifurcation may be 
treated by scraping and flowing oxyphosphate of copper cement into 
it (Figs. 646 and 647). In view of hemorrhage this may be better 
done if the gum is gently packed away with cotton and eugenol for 
a day. 

In cases of excessive loss of the pericementum to the apex of one 
root, the pulp will be infected and must be devitalized. Unless 
markedly hyperemic or evidently degenerate it is better not to dis- 
turb it when the pocket does not approach the apex, at least not as a 
routine measure. Simple hyperemia can often be recovered from. 
Sometimes such a root must be amputated if it swings free of attach- 
ment, provided the other roots will support the tooth. In view of the 
present doubt as to the success of canal treatment it may be better to 
extract such a tooth. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 671 

Rhein 1 calls attention to the fact that collections are apt to occur 
about the surface left by the amputation, and that postextraction 
resorption of the alveolar process occurs. To obviate this he suggests 
the use of a porcelain root to replace the lost root, and about which 
the tissues contract firmly and remain in a healthy condition. This 
operation Rhein terms " heteroplasty following the amputation of 
natural roots." 

Briefly outlined the process is as follows: 
%1. Prepare and fill the root canals as far as the pulp chamber; fill 
this with temporary stopping. 

2. Amputate the necrosed root by means of a fissure drill, and 
remove. 

3. Coat the root with a film of paraffin to allow for shrinkage of 
the porcelain. 

4. Take an impression of one-half of the root (longitudinally) by 
embedding in plaster; make articulating grooves and pour plaster 
for an impression of the other half; separate and remove the root 
from the plaster. 

5. Burnish matrix platinum into each half of the impression, 
stiffen with porcelain, and reburnish. Complete one side with 
porcelain as in inlay work; in the other fuse a platinum box formed 
over a square platinum pin (this pin should be left in the box until 
the packing of the porcelain about the box is complete). 

6. Flatten the proximating sides of the halves; paint with thin, 
fresh body; press together and fuse. 

7. Strip off all platinum and dress off all protruding points, coat 
the entire porcelain with a thin film of body, place in furnace in an 
upright position, and heat almost but not quite to a glaze. 

8. Wash out socket of natural root with antiseptics and remove 
temporary stopping from the crown cavity; try porcelain root in 
place, and if right dry everything; fill the box with cement, return 
the root to place, and pass the pin through crown cavity and into the 
root box. Adjust root, leaving a slight space for an amalgam joint. 

9. Pack the crown cavity and the joint with amalgam, and at a 
later sitting finish the same (Fig. 648). 

This operation does not seem to have general adoption. These 
measures so far outlined together with the grinding of maloccluding 
teeth and splinting for surgical rest constitute the so-called surgical 
method of treatment adopted by many specialists today, as the sole 
method of treatment and as inviting an outpouring of bone-forming 
material. Most of them make a point of extracting badly involved 

1 Dental Cosmos, September, 1900, and September, 1902. 



072 



PYORRHEA ALVEOLARIS 



teeth and there is much to be said for this as it removes the chief 
source of the infection, i. e., the teeth most subject to recurrence, 
simplifies the treatment and enables supporting bridges or plates, 
acting as splints, to be constructed. In all these, the demands of oral 
hygiene against oral sepsis are satisfied (see chapter on Prophylaxis, 
etc.). 

Some operators prefer to coat the gum margins with a solution 
composed of iodin crystals dissolved to solution in beechwood 
creosote, following this with a saturated solution of tannin in glycerin, 
these forming a collodion-like coating if applied with temporary 
exclusion of saliva 1 (Adair, Hartzell). 

Fig. 648 




Heteroplasty following the amputation of natural roots. (Rhein.) 

The Prevention of Excessive Motion. — The excessive move- 
ment of loosened teeth but increases the deeply seated gingivitis in 
the remaining tissues. These demand rest. Any excessive occlusion 
due to the swelling of pericemental tissue may be compensated for 
by grinding the occluding surfaces. Such excessive occlusion and 
motion are readily detected during the act of occluding the teeth 
(by noting a buckling motion), or by means of carbon paper. To 
some extent retraction of the tooth may be counted upon by con- 
traction of the pericementum in recovery due to treatment of the 
inflammation. Whether natural tightening up of teeth as above 
described may be expected to suffice or whether splints must be 
applied to temporarily aid in the cure or whether the teeth should be 



See I. Sydney Smith: Dental Cosmos, November, 1916. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 673 

permanently fixed in position as the only hope is a matter for experi- 
ence, judgment and mechanics to decide. Even trial of temporary 
splints may indicate permanent ones and they should often be con- 
sidered in the preliminary explanation of the treatment as they are 
an expensive part of the cure. The fixation of teeth is a matter of 
mechanics, and the device used depends upon the case. Slightly 
loosened teeth may be temporarily splinted with ligatures of wire 
or floss silk. To prevent the slipping of these toward the gum 
margin it has been suggested 1 that small buttons of Harvard or 
other adhesive zinc phosphate should be placed upon the labial faces 
while under the rubber dam (Fig. 649). The floss silk may be 
saturated with a solution of chemically pure celluloid in acetone 

Fig. 649 Fig. 650 






Temporary splint of silk floss or silver wire 30-gauge (one turn only shown) . Buttons 
of zinc phosphate. (Rhein.) 

(155 to 500 gr. 2 ) to render it impermeable and more lasting. The 
preparation after application is allowed to dry under the dam to a 
coagulum and then dismissed for twenty-four hours, when it may be 
polished. It lasts for several months. The wire should ordinarily 
be of brass, as it is less likely to permit caries, and may be applied 
as a single strand being woven in figure-of-eight fashion, or better, a 
single loop may be made about all the teeth to be included and smaller 
loops about the wire at the interspaces, and these twisted tight to 
effect a tightness of the first wire. The fault in ligatures is that some 
mobility is always present, due to slipping and stretching. They 
may slip toward the gum, in which case a loop or two may be carried 
over the occluso-interproximal embrasure. For certain cases Dr. 
Hugh Mitchell has suggested a bar of iridioplatinum wire adapted 
to the lingual surface of the teeth to be splinted, and soldered to 
simple gold bands to be attached with cement to two of the teeth 
adjoining the loose teeth. The other teeth are braced to the splint 
with fine wire, gold or platinum being preferred for anterior teeth. 

1 Reitz. * Kowarska's paste. 

43 



674 



PYORRHEA ALVEOLARIS 



Such a splint may be quickly made and is very effective, all slipping 
of ligatures being prevented; moreover, the wire may be kept away 
from the necks of the teeth and the gums. It can be used perman- 



Fig. 651 



Fig. 652 





Diagram showing labial view of Mitchell's 
splint, with two bands and wiring. 



Diagram showing view of Mitchell' 
splint with two bands and bar. 



ently (Figs. 651 and 652.) After a reasonable period of immobility 
the attachment secured by treatment may be tested. Very loose 



Fig. 653 



Fig. 654 



Fig. 655 






Five rings and included artifi- Two rings and included artifi- Method of making 
cial tooth. (Evans.) cial tooth. (Evans.) rings as in Fig. 493. 

teeth which have lost much of their supporting alveolar process must 
be secured by permanent splints. The simplest of these is a series of 



Fig. 656 



Fig. 657 





Labial view of a splint (see text). Lingual view of splint shown in Fig. 656. 

Fig. 658 



onnnno 

Occlusal view of the splint. 

rings soldered together, or its equivalent, shown in Fig. 650. The 
teeth are firmly ligated at their necks with floss silk. A wire measure 
is taken of the entire circumference of the teeth to be included, 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 675 

allowance being duly made for burnishing. A piece of thin platinum 
or 22 k. gold, No. 34 gauge and one-eighth inch wide, is cut to measure 
and a lap joint made and soldered. The ring is placed upon the teeth 
and moulded to their surfaces and to their interspaces. The thinnest 
separating saw is used to cut almost through the splint on both 
sides at one interspace. In this groove a straight piece of the plate 
is placed and the whole withdrawn from the teeth and the joints 
soldered. The process is repeated at another interspace and so on 
until the piece is complete. If the teeth are very tender, a plaster 
impression of the tips of the teeth may be taken and the work done 
on a fusible metal model. It is much less accurate, however. If space 
be necessary, the teeth may be slightly disked upon their proximal 
sides. If such spacing be not desirable, the necessary room can 
usually be obtained at the median interspace, but one platinum sep- 
tum is placed and the piece is to be somewhat stiffened with solder 
at the indentations representing the interspaces. To render the appli- 
ance less conspicuous the entire lingual side may be stiffened with 
solder and solder be placed liberally at the junction of band and 
septum on the labial side. Nearly all the labial portions of the bands 
except the end ones may be cut away, leaving T-buttons at the labial 
portions of the septa (Figs. 656 and 658). The teeth may loosen 
in this more readily than in that shown in Fig. 650. 

Another valuable device consists in grinding steps into the lingual 
surface of an incisor or cuspid. Soft thin metal is adapted. Three 
pins, No. 20 guage, are placed, two incisal straddling the pulp and 
one at the cervical step. The whole is stiffened with solder. Adjoin- 
ing teeth may be united by union of these plates or they may be 
used as anterior abutments of bridges. A modification consists in 
grinding the whole of the lingual enough for strength and allowance 
for occlusion, using three safely placed pins and allowing the plate 
to grasp the mesial and distal slopes of the lingual surface. This 
resists the twisting strain. 

It may also be used on centrals and cuspids. For example, in 
a case of loss of an upper cuspid and lateral the two centrals 
were fitted with the tripod step plates in Fig. 659 and 
the first bicuspid with a Carmichael, the pontic teeth fig. 659 
then attached. No pulps were devitalized. In bicus- 
pids the Carmichael attachment forms a very strong 
abutment. For example, in a case practical for several 
years two somewhat loose upper bicuspids and a some- 
what firmer cuspid were splinted with attached Car- 
michaels. These must be watched for possible subsequent caries 
which is ; however, not so great as to be prohibitive. 



676 PYORRHEA ALVEOLARIS 

Evans' method is readily comprehended by reference to Figs, 
653, 654, and 655. 

These splints are to be cemented with adhesive hydraulic zinc 
phosphate so manipulated as to set quickly. 

The foregoing splints are too conspicuous for use in some cases. 

A simple device introduced by Dr. L. C. Bryan 1 consists of a pure 
gold band about one-eighth inch wide, nicely bevelled at its edges, 
and adapted about the necks of the lower incisor teeth to be splinted 
in somewhat the same manner that the splint illustrated in Fig. 650 
is adapted. Particular attention is paid to the interspaces in the 
endeavor to bring the labial and lingual sections together as nearly 
as possible at that point. When ready the piece is sprung off, the 
rubber dam is applied, zinc phosphate is placed within the band and 
upon the necks of the teeth at all points, and the band is put in 
place and burnished. Before the cement has set gold wire is to be 
passed around the interdental portions, tightly twisted, and the 
twisted end cut off nearly to the band, and the remainder bent back 
into the indentation in the band. Dr. Bryan recommended gold 
clamps in the place of wire, but these are difficult of adaptation. 

Such a piece is to be placed only on those lower incisors about 
which salivary calculus promptly collects, and* should be avoided 
in the mouths of patients who will not present frequently for pro- 
phylactic service. Confined to such cases they do good service, and 
the cement does not readily wash away; indeed, a slight coating of 
calculus seems to protect the surface of it from solution. If the 
calculus be kept from the gum this remnant does no harm. 

Several devices have been offered which require the devitalization 
of the pulps and filling of the root canals of the several teeth to be 
splinted. 

D. D. Smith 2 suggests reduction of the lingual surfaces of the 
teeth and the fitting to them of thin metal backings, which, after 
adaptation to the teeth, are perforated and pins are thrust through 
for the root canals. After soldering each pin to its plate, readapting 
the latter and stiffening with solder, an impression is taken and the 
plates are united. The whole piece is cemented to place with oxy- 
phosphate. A modification for vital teeth would be to drill three 
safe pits for pins for each plate instead of the one central pin for 
the canal, or to drill one hole through the incisal portion above the 
pulp for each plate. With this device one or more artificial teeth 
may be included to replace lost teeth (Figs. 660 to 664). The 
incisal edges, if broad, could have individual inlays cast on two 
safely placed pins and these soldered together. 

1 International Dental Journal, 1899, 2 Dental Digest, 1902, 



Fig. 660 



Fio. 661 




Splint for securing previously treated lower 
anterior teeth. (Ames, after Smith.) 

Fig. 662 




Splint for use in the case shown in Fig. 661, 
Fig. 664 




Same as Fig. 661. Splint in position. 
Fig. 665 






Upper teeth prepared for splint. 
(Ames.) 

Fig. 663 




Root with cap fitted. (Ames ) 
Fig. 666 




Tooth with Richmond cap. (Ames.) Splint for lower incisors. (See text.) (Ames.) 



678 



PYORRHEA ALVEOLARIS 



I had a case of loose pyorrhetic incisors to be splinted with 
the pulps vital and an artificial tooth included. Following a 
radiograph two pits were drilled from the lingual in each incisor for 
reception of iridioplatinum wire, No. 20 gauge. Thin platinum 
plates were adapted to each tooth and the pins thrust through and 
soldered separately for each pin. After readaptation of each plate 
and stiffening with 22 k. solder, they were all placed in position and 
an impression taken, a fire-withstanding model made and the pieces 
united, a temporary wire looping lingually being used across the space 
for the tooth to be introduced. The whole was then placed on the 
teeth and adapted again. A new impression and bite were taken and 
a long pin facing with cast backing arranged and the latter soldered 
in place. Allowance was made for the facing to be slid in after 
setting the appliance. A Steele facing might have been used. 

Ames 1 suggests that in certain cases of lower incisors the teeth be 
devitalized and amputation be performed at the neck of each. Each 
root is then trimmed and fitted with a gold Richmond cap without 
pin (Fig. 663). 

Fig. 667 




Splint for lower incisors. (See text.) (Ames.) 

Each natural crown is slightly trimmed and fitted with a gold 
Richmond cap with a pin (Fig. 665). These two caps are united 
with wax, carried to the mouth, and adjusted in position. Each is 
then carefully removed, the natural crown laid aside (in water), 
and the gold sections invested and soldered together. The individual 
parts are readjusted in the mouth, an impression taken, an invest- 



1 Dental Cosmos, 1903. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 679 

ment made, and all soldered together. The natural crowns are then 
fastened in their prepared sockets with cement, and the piece is 
cemented to place. Pins may be placed in the roots if desired 

(Fig. 666). 

Fig. 668 




Splint and double saddle bridge combined. Front view. (Ames.) 

If desired the piece may be further attached co the adjoining 
teeth by means of the lingual plate and pin (Fig. 667). The Ames 
device would be useful in cases in which approximal cervical caries 
exists. 

It may be stated that three or four teeth fairly loose individually, 
when united together may, as a whole, be quite firm. 



Fig. 670 




Right side of extension bridge shown in 
Fig. 668. 



Left side of extension bridge shown in 
Fig. 668. 



Ames claims that the extension bridge shown in Figs. 668, 669, 
and 670 lasted for years and was in as good condition then as at the 
beginning. Fig. 668 gives the anterior view, Fig. 669 that of the 
right side, and Fig. 670 that of the left side. In view of oral sepsis 
this would not seem advisable and indeed, one should be chary of 
devitalizing teeth if possible to avoid it. 



6S0 PYORRHEA ALVEOLARIS 

Rhein offers the following: After pulp removal and root filling a 
transverse groove is cut in the lingual side of the central or loose 
teeth and a half-groove upon the mesiolingual aspect of the pier 
teeth. A staple is formed of triangular iridioplatinum wire to fit 
into the root canals of the pier teeth. To this is soldered a pin for 
each of the central teeth. The face of the wire should approximately 
fit the bottom of the groove (Fig. 671). Rhein suggests the following 
method of attachment: (1) Fill the root with a paper point, place 
cement over that, and fill the cervical margin of the cavity and its 
floor with gold; (2) drill through the gold to the paper point, remove 
it, and refit the retaining appliance; when ready set with zinc phos- 
phate, avoiding excess; (3) when this is set cut away to the gold 
and complete the gold fillings. 

A less elegant but still practical method would be to cover the 
pins with a good, color-keeping amalgam pressed into the excess of 
cement before it has set. The margins are then to be freed of cement 
and the operation completed with amalgam, which later should be 
polished. In undecayed teeth this has no advantage over the method 
shown in Fig. 660; nor in decayed teeth over that in Fig. 665. 

Smith's, Rhein's, and Ames' devices permit the use of an artificial 
tooth if necessary. The same may be said for the device which 
consists of a series of gold rings (Evans'). 

For the molars and bicuspids Rhein's device is transferred to the 
occlusal surface (Fig. 673). 

Short metal caps made for the incisal tips of lower incisor teeth 
adjoining a space will successfully hold a bridge tooth. The device 
is, however, rather conspicuous. Well anchored gold inlays joined 
by solder or cast together, or a staple in two or more roots of 
different teeth about which staple fillings are later built may be 
useful. Carmichael attachments will serve for some teeth. 

For the molar and bicuspid teeth it seems good practice to adapt 
short crowns to the teeth trimmed only to the fullest point of con- 
tour, and unite these with solder. Occasionally the bands may be 
slit occlusally and adapted closely without covering the cusps. A 
sort of bridge is thus made which causes the teeth to be firm even 
if all are originally loose (Fig. 672) . It is mainly this factor which 
renders bridge-work useful in pyorrhea alveolaris upon isolated 
teeth. If the necks of such teeth are hypersensitive, silver nitrate may 
be used. This device is especially useful when teeth are inclined. 
As an example, an upper third and second molar were fitted with 
short crowns, a first bicuspid with a Carmichael and a pontic 
bicuspid used. These united held the three loose teeth very firmly. 

The use of united barrel crowns reaching the gum margins is at 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 681 

times useful, but the configuration of exposed roots may render this 
impossible in some cases. 

By the use of pure gold crowns, which may be stiffened occlusally 
with solder to gain strength, or a 22 k. reinforced occlusal used, or a 
specially stamped clasp metal occlusal used, better adaptation at 
cervical portions may be obtained by hand burnishing after cemen- 
tation of the piece. 

All appliances cemented to the teeth and having a free margin are 
subject in some degree to a solution of the cement. These cases 
should be seen frequently in any event for prophylactic purposes, 
when the condition of the appliance may be noted. 

Extraction and bridge-work may be at once resorted to in some 
of the aggravated cases, though if the appliance be mechanically 
constructed teeth which may be extracted with the fingers may be 
firmly held in splints for years. While this is a fact, good judgment 
as to sepsis demands the early removal of such teeth before an appli- 
ance is constructed. 

If desired the bridge may be made so as to mount the natural teeth 
after their extraction, by constructing sockets of gold for the recep- 



Fig. 671 





Fig. 672 



Permanent splint for cases of pyorrhea alveo- 
laris in upper or lower incisors. (Rhein.) 

Fig. 673 

tion of the necks of the teeth 
somewhat after the manner 
employed in the Ames method. 
The sockets are then soldeerd 
to each other and to the 
bridge piers, after which the 
teeth are attached. 

These sockets are to be 
made deep at first, and it is 
well to attach the teeth with gutta-percha in order that the row of 
sockets or a new row may be lowered to fit the gum if desirable. This 
will require the raising of the teeth to the occlusal level. Occasionally 
the use of the overarch bar is demanded to prevent the overuse of the 
teeth acting as piers for bridge-work. 




Permanent splint for cases of pyorrhea alveo 
laris on molars and bicuspids. 



682 PYORRHEA ALVE0LAR1S 

E. Ewing Roach 1 has suggested that in case of loose incisors drill 
holes may be made from mesial to distal or the reverse, and a plati- 
num wire, 18 or 20 gauge, be cemented through the several teeth. 
The cases must, of course, be selected. 

The lateral support of teeth by plates is occasionally of use in 
pyorrhea, but the question requires careful consideration. (See 
page 591.) The prevention of mobility in advanced cases may be 
at times an impossibility. In such cases extraction, and the use of 
artificial teeth or of bridges, is probably better judgment than the 
retention of the teeth until extracted one by one. In all cases the 
element of overuse must be considered and anything possible done 
to prevent it. (Read carefully pages 588 to 593.) Also anything 
that may induce gingivitis, as a riding plate festoon, must, if 
possible, be avoided. 

Medicinal Treatment. — Simple cases often heal spontaneously after 
thorough work and antisepsis. If aseptic a clot drawn after the irri- 
gation of the pocket with hydrogen dioxid is often useful. Some 
operators depend upon blood flow, the calculus being fished out with 
clot as the work proceeds. In order to control the patient and watch 
the case, any pocket existing after a week should be washed out with 
hydrogen dioxid and then filled with balsam of Peru which can be 
kept ready at hand in a Safety Sub. Q syringe. This substance is a 
mild antiseptic stimulant of a viscidity sufficient to fill the pockets 
even though wet, if the needle is inserted to the bottom. Thereafter 
it should be used twice a week. 

If the case refuse to heal there may be calculus overlooked upon 
the roots. An acid is used to soften this if not removable by instru- 
ments. Head recommends the use in the pockets on each fourth 
day of ammonium bifluorid 2 as a solvent of calculus and tissue 
stimulant. It does not dissolve enamel or cementum. The tissues 
are to be protected against burns from any overflow, which must be 
removed. It produces no harm within two minutes. It is to be 
injected with a rubber syringe with a platinum point (Dunn syringe). 

Lactic acid full strength (Younger), trichloracetic acid, 25 per 
cent, strength (Kirk) ; sulphuric acid', 25 per cent, strength (Truman) 
are all solvent for tartar, and stimulant germicides if infection con- 
tinues the ulceration. The applications are made once or twice a 
week until suppuration ceases and the pockets are closed. 

1 Dental Cosmos, 1908, p. 65. 

2 "Tartar Solvent," or "Tartasol," is made by neutralizing hydrofluoric acid with 
ammonium carbonate, filtering, evaporating to half the bulk, adding again an equal 
bulk of hydrofluoric acid, and again evaporating to one-half bulk (at 90° to 105° F.). 
(Items of Interest, 1909, p. 175.) 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 683 

As an astringent antiseptic zinc chlorid deliquesced, or sulpho- 
carbolate of zinc in 10 per cent, solution, or zinc iodid in 10 per cent, 
solution, or copper sulphate, 10 per cent., or powdered copper sul- 
phate are all useful. 

As an astringent lotion, zinc chlorid, gr. x to each fluidounce of 
aquse rosae, aquae gaultherise, aquse menthi piperitse, etc., may be 
applied by the patient daily on a cotton swab made by rolling cotton 
on the end of a tooth pick. It may be diluted to an agreeable astrin- 
gence for a mouth wash (or two-minute bath), or tincture of iodin 
may be applied every other day, or iodoglycerol (see page 678) may 
be painted upon the gums every other day by the dentist, iodoglycerol 
diluted 1 to 3 with water may be applied daily by the patient or may 
be diluted 1 to 500 as a wash. 

Gentle massage of the gums by means of the finger-tips stimulates 
the tissues and squeezes out secretions. If common table salt be 
used in conjunction the stimulant antiseptic effect is obtained. 
Powdered sulphur is recommended by Gordon White instead. 

The use of a strong stream of water from a syringe is recommended 
by Black to wash away the agglutinin collected. His use of this 
alone has been condemned by experienced periodontitists. 

Dr. A. B. Harrower has suggested the following formula for a 
powder which has in his own and my hands given good results as an 
astringent antiseptic: 

Ifr — Magnesium carbonate lb. j 

Cream of tartar lb. iss 

Red cinchona bark 5ij 

Calcined alum 5J 

Oil peppermint f5v 

Oil cinnamon f 5iij 

Oil rose geranium f 3 j 

All ingredients to be finely powdered. The oils are to be added to the magnesium 
before thorough mixing of the powders. The whole is to be sifted through silk. 

Saccharin may be added to the above as a sweetening agent. The powder when 
wet is almost neutral, and should do no harm in its limited use as a therapeutic agent. 
I have also had good results from the alternate use of Pepsodent Tooth Paste as a 
cleanser and Pyorrhocide Tooth Powder, especially if a special brush made from a 
pointed polishing brush held in a Jack porte polisher is occasionally used. (See Pro- 
phylaxis.) 

Black has recommended the use of the 1-2-3 mixture, or phenol- 
camphor, to be put into the pockets every three days, and a few 
drops to be used on the tooth brush. 

1$ — Oil of cinnamon 1 part 

Carbolic acid 2 parts 

Oil of gaultheria 3 parts 

]$ — Gum camphor, 

Crystal carbolic acid aa q.s. 

Mix in a mortar to an oily fluid. 



684 PYORRHEA ALVEOLARIS 

Barrett 1 injects as an ainebacide in cases showing endamcebse a 
one-half of 1 per cent, solution of emetin hydrochloric! in normal 
saline solution into the tissue at the bottom of a pocket and fills the 
pocket with the solution, repeating this on several consecutive days (see 
page 712). The scaling is not all done on each tooth at once by him, 
but repeated on the successive days. He finishes the treatment with 
1 per cent, iodin in normal sodium chlorid solution as a bactericide. 

The solution must be freshly made and limited to J grain at each 
treatment to prevent nausea. He agrees to hypodermatic treatment 
with Emetin at the end of the course to reach unknown foci. If 
complicated with spirochetal infection treat locally with some one 
of the arsenical preparations, as neosalvarsan or arsenobenzol. 

Regeneration in the pockets should not be disturbed, so that 
unless the pus flow be active one should wait until sufficient time has 
been afforded (about a week or ten days) for granulations to form. 
If pus be then detected the pocket should be again treated thoroughly. 
Good results are obtained from the use of an astringent antiseptic 
wash used in forcible spray from an atomizer or introduced by means 
of a syringe. This should be done daily by the patient. (See 
Asepsis.) Stagnant fluids in the pockets are washed out and 
replaced by the antiseptic, thus inhibiting the bacterial growth in 
the pockets and the mouth. 

The teeth should be cleansed after meals to prevent media for 
infection lodging about the interstices, after which the antiseptic 
spray will aid in inhibiting bacteria. If the case still refuse to heal 
Beck's bismuth paste may be used. 

]$ — Bismuth subnitrate 30 parts 

White wax 5 parts 

Paraffin 5 parts 

Vaselin 60 parts 

Mix while boiling. 

It is injected from a syringe kept for the purpose. 

Good results from the application of the a:-rays and high-frequency 
currents have been claimed by Parker, 2 Price, Guy, Satterlee, Tousey, 
and others. 

Raper claims that the otherwise incurable cases are not benefited, 
and there is also some danger in repeated applications of .-r-rays. 

Sturridge 3 has shown that antiseptic ions may be introduced into the 
overlying gum tissue to the depth of 4 mm. with 5 ma. of electrolytic 
current in three minutes. He favors 3 per cent, zinc chlorid solution 

1 Dental Items of Interest, 1915. 

2 Dental Cosmos, December, 1903. 

3 Ibid., 1916, p. 403. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 685 

and 3 to 15 ma. positive pole in the gum trough as checking pus 
formation and improving the tone of the tissues, when conjoined 
with the approved mechanical treatment as previously outlined. He 
notes the disappearance of alimentary toxemia, toxic neurasthenia, 
rheumatism, arthritis, etc., under this treatment as a result of cure 
of pyorrhea when dependent upon it. Fette claims good results 
from the use of a small copper spatula positive electrode, used 
without any liquid, for the purpose of introducing copper ions until 
the tissues are colored blue. 

The high-frequency currents are applied by small vacuum tubes 
or electrodes directly to the gums. They contain and emit violet 
and ultra-violet rays, which not only stimulate the part through the 
electricity, but also produce ozone upon the gum surface and carry 
it in and also produce ozone in the tissue by electrolysis. 

The production of Bier's hyperemia by suction upon the tissues 
is attributed to Keefe 1 by Cazier. Prinz and Colyer also recommend 
it. Cazier has introduced a method of general suction by means of a 
rubber cup somewhat like an impression tray, having a tube attached 
to fit over the entire arch and alveolar gums. A vacuum is created 
by means of a suction apparatus attached to a water faucet and 
operating like a saliva ejector, a rubber tube and a secretion catching 
bottle are the connecting media. It is known as the "Sanitor." 
The strong vacuum to be made daily evacuates the infected secre- 
tions in the pockets, and induces a flow of healthy secretions, and 
induces a hyperemia increasing the opsonic index of the fluids of 
the tissues and the number of healthy phagocytes. 

The cups sold sometimes do not fit, especially with long teeth. 
The writer then takes a modelling compound impression, makes a 
model (Fig. 674), builds the teeth up with plaster, but keeps it away 
from the parts representing the gums to be covered. Over this while 
warmed a broad sheet of Para vulcanizable rubber 2 is adapted with the 
fingers and an extra layer placed where stiffening is required (not at 
the flanges). A tube is inserted in place and the whole vulcanized 
for thirty-five minutes at 317° F. A box flask may be necessary. 
This is to be used by the patient twice a day at the beginning, once 
a day later, then perhaps every two or three days as a prophylactic. 

Good results have been obtained in some cases by extraction and 
replantation, after root preparation and sterilization of the tooth and 
alveolus. The alveolus may have to be deepened. The method is 
open to question. 

There sometimes appear pus pockets or periodontoclasia with 

1 Dental Items of Interest, December, 1916, p. 927. 

2 Obtainable of the S, S. White Dental Mfg. Co. 



686 



PYORRHEA ALVEOLARIS 



or without pocket on a few teeth in mouths, that while attended to 
have gradually gone through poor operative procedures, especially 
such as are due to extractions or poor contours. These should be 



Fig. 674 




Very persistent case of pyorrhea, in a young man, aged twenty-five years, apparently 

vigorous. 

looked after and the mechanical conditions corrected. They are 
sometimes more annoying than new and frank cases of pyorrhea. 

Prophylaxis.- — This is all-important, especially in the cases in which 
chronic disease or malnutrition may not be readily overcome owing 

Fig. 675 





Method of building up the model in Fig. 674 with plaster; ready for covering with 

vulcanite. 



to confirmed habit of life or advanced stage of disease. The local 
conditions existing even after a cure of pyorrhea are such as to invite 
reinfection, and the establishment of microbic plaques, which frequent 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 687 

cleansing of the teeth will remove. The system of monthly or, if 
necessary, more frequent prophylaxis advocated by D. D. Smith 
should be practised. Its good results are particularly manifest in 
this class of cases. Also the use of the prophylactic stick or brush 
by the patient twice a week and the careful and proper use of floss 
is very beneficial. The patient performs these manipulations with 
difficulty, and is apt to backslide. (See Prophylaxis.) 

Recurrence of the condition is probable if the oral prophylaxis or 
systemic treatment be neglected. The simpler cases yield quite 
readily; the advanced ones, in which much of the alveolar process 
is lost, and especially when the gums are flabby and admit food to 
the pockets, tax the patience of operator and patient alike, and are 
apt to end, sooner or later, in loss of the teeth affected. 

Fig. 676 




Showing flexible cap and its tube for connection with suction apparatus. Vulcanized 

over model in Fig. 675. 

This fact, however, should not prevent the retention of these 
teeth by every means at command during the period for which 
they may be made useful. If, however, any tooth prove an incurable 
source of pus formation, or from the first be likely so to do, it should 
be removed, otherwise the remaining teeth, and possibly the patient's 
blood, are continuously infected. 

Summary of Treatment. — It is not expected that one will employ 
all the methods here" outlined, but the following routine may be 
employed : 

1. Sterilization by sprays or especially Talbot's iodoglycerol with 
resterilization of instrument and pockets by using the quarter 
strength iodin on the scaler as one scales. No serious objection 



688 PYORRHEA ALVEOLARIS 

attaches to the use of local anesthetics if needed to avoid pain though 
usually not needed. 

2. Thorough scaling of such teeth as are operated upon, removing 
all particles from the pockets and inducing a final clot. 

3. Keeping the parts aseptic and constringed by use of Talbot's 
iodin quarter strength applied on swabs by the patient and the use 
of the same well diluted as a general wash. 

4. The continuance of the treatments upon other teeth with 
reattention to the first pockets, if not healed after say ten days, 
especially if suppurative. 

5. The use of medicament in the pockets, if preferred or needed. 
Systemic treatment in bad cases. 

6. Attention to the prophylaxis by the patient and periodic pro- 
phylactic treatment as needed. 

If preferred one may take up another technic, Barrett's, for example, 
first making the microscopic diagnosis and pursuing this line of 
thought throughout then following up the cure by prophylaxis 
against recurrence. 

Systemic Medication. — Various methods of systemically attacking 
the infection existing in the tissues about a pyorrhea pocket have 
been introduced. 

These aim to either (1) destroy the bacteria or endameba? by 
introducing into the blood in various ways certain antagonistic 
chemical substances which shall finally find their way to the tis- 
sues involved and there act as amebicides or bactericides. (2) To 
constringe the tissues thus reducing their volume and amount of 
liquid, thus probably increasing the phagocytic power. (3) To raise 
the general leukocytic count and probably the opsonic index, or to 
stimulate phagocytic activity through the opsonins by means of 
vaccines. (4) To raise the standard of health by counteracting morbid 
nutritional processes thus increasing resistance, improving the quality 
of blood and its leukocytic activity and probably its opsonic power. 

These objects will be considered serially as Xos. 1, 2, 3 and 4. 

Object No. 1. — Three methods are under consideration at the 
present time: 

(a) The use of emetin as antagonistic of endameba? (buccalis or 
Kartulisi). The hypodermic injection of emetin hydrochlorid was 
introduced by Bass and Johns 1 following the local use by Barrett, 
and the suggestion by Smith of the. possible use of hypodermic 
medication and both based upon the demonstration by Eogers of its 
value, hypodermically against amoeba hystolytica in the alimentary 

1 Text-book on Alveolodental Pyorrhea. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 689 

canal (amebic dysentery). They employ the following technic: A 
sealed ampoule containing \ grain in sterile solution is broken at the 
neck and the contents drawn into a sterile hypodermic syringe. A 
point over the insertion of the deltoid muscle (or wherever the skin 
is loose) is sterilized with pure lysol applied on moist (not wet) cotton 
on an applicator and the injection made fairly deeply and intra- 
muscularly or well beneath the skin. The needle is withdrawn and 
the lysol wiped off. This is done for six consecutive days. Redness, 
soreness, itching, some possible formation of small vesicles, shedding 
of epithelium are probable or possible. Some urticaria, usually mild, 
in about 1 per cent, of cases. 

They expect endamebse to disappear from the tissues in about three 
to six days from the initial injection. Eisen and Ivy 1 report good 
systemic results as well as local by a course of \ grain injections for 
six consecutive days. Local treatment follows. A second course 
after a week or two is given if endamebse are still present and pro- 
phylactic injections at a later date. 

Alcresta Ipecac. — A tablet has been prepared by Eli Lilly & Co., 
each containing the alkaloid of 10 grains of ipecac held in adsorption 
in a colloidal form of hydrated aluminum silicate to render it insol- 
uble in the acids of the stomach, but set free in the alkaline juices 
of the intestines. The chances of nausea are reduced though some 
purgative action ensues (Lloyd). Emetin is absorbed into the blood. 
Bass and Johns accredit it with causing disappearance of endamebre 
from the pyorrhea pockets about as quickly as the hypodermic 
method. 

Three tablets are given three times a day until about 40 are 
taken. 

(b) The Use of Succinamide of Mercury. — Dr. Barton S. Wright, 2 
Surgeon, U. S. N., in 1910 introduced the above preparation, to be 
injected intramuscularly preferably into the buttock by means, of a 
Burroughs and Welcome 40 m. all-glass intramuscular type syringe, 
with 1J inch needle, No. 26 platinum iridium. Each § grain tablet is 
dissolved in 4 mils, of water. 

The dosage is f gr. or f gr. initial, followed by | gr. or -f- gr. seven 
days later or f gr. if idiosyncrasy appears; women require \ gr. or \ 
gr. less per dose. 

The buttock is painted with iodin and allowed to dry. The needle 
is held by the hub between the thumb and forefinger about a foot 
above and quickly thrust to the hub into the gluteal muscle practi- 
cally without pain. The syringe filled with the desired solution is 

1 Dental Items of Interest, February, 1916, p. 103. 

2 Dental Cosmos, September, 1915, p. 1004. 
44 



690 PYORRHEA ALVEOLARIS 

attached and a steady injection made, the needle withdrawn and the 
puncture touched with iodin. 1 

Uniform improvement and cure of pyorrhea and its systemic 
sequelae is claimed when local measures are also used which 
Kritchersky and Seguin 2 confirm. 

(c) The Use of Neosalvarsan. — Kritchersky and Seguin inject in- 
travenously 10 to 30 centigrams of neosalvarsan and claim their dis- 
appearance when spirochetes are present in pockets as is usual, with 
good results when local measures and prophylaxis are conjoined (see 
page 654). In syphilitic cases Wright also uses this for the arthritis. 

When contra-indicated they use succinamid of mercury as above. 

Object No. 2. — This is accomplished by the use of vasoconstrict- 
ing agents, especially dilute sulphuric acid, in doses of 15 to 20 
drops per orem three times a day as long as needed. 

Object No. 3. — (a) Waas 3 has suggested the aseptic injection sub- 
cutaneously of 2 mils, of a 10 per cent, solution of sodium nuclein salt 
in physiological salt solution as capable of raising the leukocyte 
count about 100 per cent, from which point it decreases during three 
weeks to a normal level. He states that sterile ampoules are prepared 
by Merck & Co., also he did not find it to have germicidal properties; 
that it i s harmless and a general phagocytic remedy for exceptional cases. 

(b) Vaccines. — A vaccine as practically applicable consists of a 
culture of the bacteria causing an infection, held in suspension in a 
liquid vehicle, standardized as to numbers in a given quantity (minims 
or mils.) and the bacteria killed by heat. 

The dead bacteria contain toxin which cause a cell reaction and 
exudation of antibodies, from the body cells, antagonistic to the 
specific bacterium or bacteria used. Being dead the bacteria cannot 
cause an infection when injected into the body. In brief, the object 
is to cause such a reaction, increase the opsonic power of the blood 
plasma and thus enhance the power of the phagocytes. 

Two forms of vaccines are used: 

(a) Autogenous Vaccines. — The infections are examined micro- 
scopically the specific bacteria decided upon, pure cultures or mixed 
as desired made,, sterilized, standardized and injected. The object 
is to use the cultures of strains actually causing the infection as being 
more likely to produce antibodies specific for the invading bacteria. 
Thus if pus formation persist and staphylococci be found as the pre- 
vailing infection, these are isolated, cultivated and used for the vac- 
cine; likewise several may be used and mixed. The examination 

1 White: Dental Items of Interest, June, 1916. 

2 Dental Cosmos, 1918, p. 782. 

3 Dental Items of Interest, May, 1918. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 691 

may be made and the vaccine made before local treatment is insti- 
tuted, though it would seem that treatment for a short time would 
eliminate the secondary infections in the pockets. 

(b) Stock Vaccines. — These are usually made from a variety of 
strains of bacteria of one species (e.g., streptococci) obtained from a 
large number of disease foci, and preferably including several pyorrhea 
cases, or a number of species of bacteria are obtained when infections 
may be mixed. Having selected the desired bacteria, these are cul- 
tivated and a vaccine prepared as above, standardized as to numbers 
in a dose, sterility preserved with J of 1 per cent, trikresol or phenol 
and sold in sealed containers, usually those sealed with rubber 
stretched over the mouth of the phial and through which the needle 
is thrust or the container and needle are combined. If kept in a cool 
place the contents are good for about a month. When drawing into 
the syringe the phial is inverted. Stock vaccines are either such 
cultures suspended in sterile salt solution without sensitization and 
known as bacterins or the bacteria are additionally subjected to the 
influence of serum drawn from an animal treated with large doses 
of the plain vaccine or bacterin until the blood of the animal is full 
of the specific amboceptors. These amboceptors (antibodies) act upon 
or sensitize the bacteria saturating them with the specific antibodies 
" so that they do not absorb antibodies from the patient, preventing 
unfavorable local or general reactions or the so-called negative phase 
(caused by bacterins), and produce effective, active immunity in 
twenty-four to forty-eight hours which is reasonably durable." 
The preparations so sensitized are called sensitized vaccines (sero- 
bacterins by the Mulford laboratories). Mulford laboratories pre- 
pare what is called pyorrhea serobacterin Mulford containing pneu- 
mococcus, streptococcus (various strains), Micrococcus catarrhalis 25 
millions each, Staphylococcus albus and aureus 100 millions each, 
bacillus influenza? and diphtheroid bacilli 50 millions each (other 
syringes in multiples of these). 

Autogenous vaccines require some time to produce; stock vaccines 
are ready for use and if prepared by a reliable laboratory safe for 
immediate administration. 

Considering the varieties of causes of pyorrhea suggested as the 
result of the findings of bacteriologists as outlined in this chapter. 
It will be seen that all that has been discovered by the use of vaccines 
is that they lessen symptoms of suppuration and cause some cures 
in cases not too hopeless when conjoined with rigid local treatment. 

It is plain that acute forms of suppuration require immediate 
treatment; local, surgical and antiseptic measures and that stock 
vaccines only are applicable. 



692 PYORRHEA ALVEOLARIS 

In chronic cases a choice may be made and, as stated, it would seem 
advisable to treat locally and employ for an autogenous vaccine such 
persistent bacteria as are cultivable or to use the stock vaccine 
indicated by such bacteria as are found on microscopic examination. 

If marked systemic infection be found, as indicated on page 555, 
such an examination should be made and the mixed varieties of 
bacteria found cultivated for an autogenous vaccine, or if urgent an 
appropriate stock vaccine used at once, partly as a prophylactic 
against general infection as the result of local disturbance of the 
infected tissues and largely to antagonize the systemic infection. 
During this treatment the autogenous vaccine may be prepared. 

The Evidence for Vaccines. — McGehee 1 claims about 50 per cent, 
of cases improved markedly through the use of the Van Cott stock 
vaccines, of which each bulb contains in 1.0 c.c: Streptococcus, 
50,000,000; bacillus coli communis, 100,000,000; pneumococcus, 
100,000,000; staphylococcus (combined aureus, albus, and citreus), 
500,000,000, killed and in sterile solution. 

He claimed his best results were obtained by beginning with one- 
fourth of the bulb content, 0.25 c.c, injecting at four-day intervals, 
later increasing to 0.50 c.c, and up to six, seven, or eight injections 
all told. 

Medalia 2 claims that in his hands autogenous vaccines com- 
bined with the corresponding stock vaccine have greatly aided in 
the cure of the local and systemic symptoms. His stock vaccine 
is prepared from bacteria obtained from various sources including 
several strains of each species obtained from pyorrhea cases and 
states that his cases were usually treated with pneumococcus and 
staphylococcus stock while the autogenous was also used, as he 
believed pyorrhea due to a largely mixed pneumococcus and 
staphylococcus infection implanted upon a mechanically prepared 
area. The autogenous vaccine includes the predominating bacteria 
specially prepared from the pus of the patient. His reason for 
the combination is the fact that autogenous bacteria are sometimes 
incapable of exciting the formation of antibodies owing to having 
been affected in degree by their host. He begins with 30 to 50 
millions, increasing every two to four days (or when reaction has 
totally or partially subsided) by 12 to 25 millions up to a maximum 
of 400 millions or until a local inflammatory reaction is produced. 
In marked reactions the dose is decreased by 12 to 25 millions. 

Head 3 cites cases of marked improvement in cases of pyorrhea 

!• Dental Cosmos, September. 1912. 2 Ibid., 1913, p. 708. 

3 Jour. Am. Med. Assn., December, 20, 1913; Text Book of Modern Dentistry, p. 
101. 



PYORRHEA ALVEOLARIS AS A MARGINAL GINGIVITIS 693 

associated with systemic conditions, (a) septic anemia with red 
cells, 3,616,000, leukocytes, 4500 with microcytes, macrocytes and 
poikilocytes, hemoglobin 30 per cent, as cured by local treatment, 
raw eggs three times a day and a vaccine (1 diphtheroid, 1 pig- 
mented streptococcus, 1 non-hemolytic streptococcus) given once 
a week. The blood result was hemoglobin, 50 per cent.; reds, 
4,000,000; leukcocytes, 9000. (6) Two cases of osteo-arthritis, 
unable to walk or use muscles as result of pyorrhea, as satisfac- 
torily improved by local treatment (with some extraction) and 
the persistent use of autogenous vaccines once a week. 

The Evidence Against Vaccines. — A. H. Merritt, 1 enjoying the 
advantage of a previous large experience with vaccines in this connec- 
tion, claims that he has found no advantage in their use as against 
strict local treatment, making the exception that the bacteria found 
in the pockets may be saved or utilized for the purpose of antago- 
nizing with an autogenous vaccine any accompanying systemic 
complications. He bases this opinion upon his results with the local 
treatment alone as compared with those conjoined with use of 
vaccines. 

Patterson 2 uses no systemic treatment beyond that required for 
conjoined systemic conditions at the hands of the medical practitioner 
and claims good results. 

All observers claim that exact local treatment must be used or 
results are not obtained. This at once throws open the question as 
to the real cause of the cure. Only when this persistently fails and 
a cure results from the use of systemic treatment (any sort) can 
this be adjudged a necessary feature of treatment in cases not com- 
plicated by systemic conditions which is a different question. 

By this it is not meant to argue against such treatment, but experi- 
ment with a series of uncomplicated cases should be tested by com- 
petent observers, first with local measures then with vaccines, etc., 
to determine the value of such as a sine qua nan. In many cases 
local treatment has sufficed to cure systemic conditions. It is noted 
in all cases of hypodermic medication, emetin, vaccine, succinamid 
of mercury, etc., that an induration may occasionally remain for 
some time about the site of injection. Likewise it occasionally occurs 
in apical abscess, so probably it is due to a productive inflammation 
the result of irritation. Head 3 regards this in case of vaccine as 
indicating " that the potentialities of the vaccine injection have not 
been exhausted," and advises temporarily withholding reinjection 
or smaller doses; also massage for absorption of the induration. 

1 Dental Cosmos, 1916, p. 62. 2 Text-book of Operative Dentistry. 

3 Text-book of Modem Dentistry, p. 99. 



694 PYORRHEA ALVEOLARIS 

Head, modifying Allan's suggestion, gives 1 ounce lemon juice 
three times a day (about 34 grains citric acid) to soften the lymph 
wall about a pyorrhea pocket to assist the vaccine in its local effects. 
Kusel 1 suggests curettement and the use of sodium cinnamate 5 
grains internally to assist phagocytes in reaching local tissues. He 
also claims that vaccines have effect on the character and deposition 
of calculus. 

Object No. 4. — The raising of the standard of health is a medical 
problem involving the entire range of malnutritional diseases. In 
view, however, of the toxic and infective effects of pyorrhea and apical 
abscess or granuloma, discovery and removal of cause should often 
lie with the dentist though physicians are alive to the possibilities 
of disease from teeth. 

Pyorrhea shares the evil honors equally with apical abscess. 

Causes of systemic disease removed the patient may often recover 
without the assistance of vaccines which have at times proved dis- 
appointing but may be resorted to. In addition the services of an 
intelligent physician are advisable in the treatment of conditions 
which may be the consequences of dental disease, but outside of a 
dentist's range of practice which is properly confined to the treatment 
herewith indicated. Intelligent cooperation will be found practically 
and ethically satisfactory. Certain general lines of treatment may 
be found on page 624 and need not here be repeated. 

SYSTEMIC EFFECTS OF PYORRHEA ALVEOLARIS. 

It has been abundantly shown by Hunter and others that the pus 
of pyorrhea and other intense oral sepsis even apart from apical 
infections is a source of systemic infection, producing effects ranging 
from gastritis to actual septic infection. The importance of this 
fact is not to be lost sight of, and patients are to be informed of the 
dangers of constant pus formation as well as of the presence of other 
forms of sepsis about the mouth and teeth. In this connection 
salivary calculus, generally unclean teeth, bridges and plates holding 
mucous collections, offstanding edges of crowns collecting food and 
mucus, and the septic cement under crowns are of importance as 
well as gum crevices and pyorrhea pockets. 

R. D. Watkins, M.D., has examined the blood of pyorrhetic 
patients, and has found a mild condition of septic blood similar to 
but less than found in puerperal fever and advanced carcinoma and 
in other infective conditions. 2 

1 Dental Cosmos, February, 1919. 2 Items of Interest, 1904. 



SYSTEMIC EFFECTS OF PYORRHEA ALVEOLARIS 695 

Goadby 1 reports the cure of a case of profound muscular weakness, 
mental depression, and insomnia after unavailing general medical 
treatment for neurasthenia, as following the extraction of teeth 
affected by pyorrhea. Craige 2 believes mental diseases are due to 
pyorrhea and have been cleared up by its cure. Vanel 3 cites a case 
of chronic septicemia with symptoms of pallor and asthenia, and 
ecchymotic patches (see page 28) on the legs, associated with pus 
formation about the roots of teeth. The symptoms disappeared in a 
few weeks after the oral treatment. Persistent headaches have been 
associated with it. 

Hunter and Leith 4 have described cases of subacute and chronic 
catarrh of the stomach and phlegmonous gastritis due to the ordinary 
pyogenic cocci, such as are found in the mouth, and which the gastric 
juice of the stomach of the particular individual at least was not 
competent to kill. Considering the fact that an oral subacute 
catarrhal condition is established in pyorrhea and that bacteria are 
capable of multiplication at a rate of each twenty or thirty minutes, 
the local transfer of the infection is not surprising. Park 5 believes 
many cases of appendicitis to be due to oral infection. 

Kirk adds to this list pernicious anemia, bronchopneumonia, 
malignant endocarditis, pyemic lymphadenitis, etc., as possibilities 
of secondary infection or extension by natural contiguous channels. 

Hartzell 6 claims that three deaths from septic endocarditis were 
traceable to violent pyorrhea. 

Medalia cites cures of chronic nasal, pharyngeal, laryngeal, gastric, 
intestinal, rheumatic, arthritic, skin eruptive and diabetic disease 
singly or in combination as cured or markedly improved by the cure 
of pyorrhea. 

Skinner instances a case of intestinal infection, accompanied by 
nervousness and weakness, with confinement to bed for three months, 
as rapidly and steadily improving after the treatment of a pyorrhea 
with profuse suppuration. Rheumatism and even arthritis defor- 
mans have been claimed as associated with pyorrhea, the infection 
and toxins being absorbed by the lymph channels associated with the 
teeth. Rheumatic fever has cleared up on removal of pyorrhetic 
teeth. The bacteriology of this relation is now being investigated. 
The organism most often offending is the Streptococcus viridans, 
which may be isolated from the blood of the patients suffering from 

1 International Dental Journal, July, 1902. 

2 Quoted by Wright: See Dental Cosmos, November, 1916. 
s Dental Cosmos, 1908, p. 192. 

4 Transactions Odontological Society of Great Britain, International Dental Journal, 
1899. 

•Surgery by American Authors. 6 Dental Cosmos, 1908, p. 240. 



690 PYORRHEA ALVEOLARIS 

a general infection due to a local focus of infection, whether this be 
in the appendix, tonsil, or a dental abscess or pyorrhea pocket. 
Hartzell states that a small pocket can keep up a systemic infection 
once it is established. It grows upon blood agar with a green color 
in its colonies. Park and Williams claim a variety of strains. If 
the same bacteria can be isolated from the blood and the focus and 
the condition clear up upon removal of the latter, the relation is 
absolute. In brief it seems to share equally with apical granuloma 
the evil honor of causing disease. It requires much courage to advise 
the loss of teeth and lines of dental work in cases of minor systemic 
symptoms, when the loss involves a large line of subsequent work, 
but in view of the apparent demonstration, that even slight pyor- 
rhea pockets may maintain a systemic infection, the possible con- 
nection should be pointed out to the patient and at least the worst 
teeth removed and others vigorously treated. Physician and dentist 
should advise together to endeavor to eliminate systemic compli- 
cations. Unfortunately a physician's statement, even when based 
only on general principles and without definite knowledge of a case, 
is often accepted as final when the most potent arguments of a dentist 
are unconvincing. The neglect of conditions tending to pyorrhea 
and of actual pyorrhetic conditions is one of the commonest over- 
sights of dentists due in part to the lack of understanding on their 
part and of appreciation of their mouths by patients. (See page 555 
and Prophylaxis.) 



PYORRHEA ALVEOLARIS NOT DEPENDENT UPON CALCULUS 

FORMATION. 

A form of pyorrhea occurs in which calculus does not seem to be 
the exciting or contributory cause. It seems rather to be due to 
infection localized in soft bacterial collections in localities protected 
from ordinary friction. 

Sometimes no perceptible calculus can be found upon the roots, 
but a soft gummy collection may be noted. The forms of the necks 
of the teeth readily permit bacterial collections and the infection 
causes a bright red marginal gingivitis, sometimes localized to a single 
portion of the gum margin. A pocket forms and the infection becomes 
deep. The gum tissue is sometimes destroyed between two teeth. 
There is often evidence of infection of other gum margins with the 
bright red color. In another form the gum margins are separated 
from the teeth. Pockets are formed which collect food. There is 
not much pus apparent, but there is a pigsty odor of putrefaction. 



PYORRHEA ALVEOLARIS 697 

The marginal bone is lost. In another form a deep pocket forms and 
necrotic bone may be found. 

The advance of the disease is sometimes rapid and sometimes not. 
Sometimes a lateral abscess is associated with it. The diagnosis is 
that of pyorrhea alveolaris of aggravated type, and probably special 
infection, and its progress, diagnosis, symptoms, and treatment are 
practically the same as in the first class. 

The advance of the case may be very slow and limited to the 
teeth originally involved. The following is an example: 

Miss H., aged twenty-five years, presented with well-established 
pockets, extending one-half inch toward the apex, upon the mesial 
aspect of the root of the right upper central incisor and distal and 
distobuccal aspect of the right upper lateral incisor. There was a 
history of traumatism due to violent and persistent wedging with 

Fig. 677 




Pyorrhea alveolaris without calculus. Pockets as shown. Teeth were one-sixteenth 
inch longer, but have been shortened. Practically no calculus and but slight flow of 
thick, creamy pus. Gum prominent over affected teeth. Condition in 1904. 

rubber at about the age of sixteen. The case was then of several 
years' standing, and the two teeth elongated about one-eighth inch 
beyond their fellows (Fig. 677). There was no subgingival calculus. 
The pockets were treated with some benefit, and the teeth shortened 
for the cosmetic effect, but the patient left the city suddenly before 
recovery, and was not seen again for three years. At this second 
visit it was found that the pockets were nearly the same as at first, 
and no other teeth had become involved. Nor had the teeth further 
elongated. 

During the four succeeding years, elongation and grinding reduced 
nearly all the brown of the lateral, which had one-quarter inch of 
its root cervix exposed. Coincidently with the exfoliation the pockets 
disappeared as though by a drawing up of the bottom. The two 
teeth were finally lost. 



CHAPTER XXII. 
PERICEMENTAL ABSCESS. 

In comparatively rare cases there begins in the lateral aspect of a 
pericementum a swelling which finally discharges its contents either 
at the gum margin or directly through the gum tissue. 

The pulp of the tooth may be perfectly vital and the attachment at 
the gum margin at first at least practically unbroken. A deposit of 
calculus may or may not be formed in the area, and the discharge may 
consist of a glairy fluid or of purulent matter. Cases of this disease 
have been noted and described by Darby (1874), W. E. Walker 
(1895), Talbot 1 (1896), D. D. Smith (1897), and Kirk (1898). Black 
claims that he has never found such a condition without local injury. 

Forms of Pericemental Abscess. — There are four forms of perice- 
mental abscess as described and seen : 

1. An ordinary pyorrhea begins at the gum margin and extends 
into the alveolus at the expense of the pericementum. The bacteria 
find their way to the bottom of the pocket or into the tissue at its 
side. They develop in the said location and the pus burrows into 
the lateral gingival tissue, causes swelling and pointing, and dis- 
charges at the lateral gingival aspect or analogous situation. (See 
page 662.) This is not always opposite the gum orifice of the pocket. 
(See Figs. 638 and 639.) In one case a fistula was found at the buccal 
aspect of the gum opposite a point midway between the buccal roots 
of an upper molar at the middle third of the roots. The pulp was 
exposed and vital, having been drilled to on the supposition of its 
death. A gum pocket was found at the distolingual aspect of the 
lingual root and the pus had burrowed into the bifurcation between 
the lingual and distobuccal root, and discharged as stated, remain- 
ing as a chronic abscess. There is a simple acute condition of this 
kind of origin seen occasionally. A swelling of the gum margin 
occurs and pointing occurs, lancing usually demonstrates pus present 
and effects a cure. The infection has entered the gingival space, 
travelled into the tissue and developed what may be termed a true 
marginal gingival abscess. 

1 International Dental Journal, 1896. 
(698) 



PERICEMENTAL ABSCESS 699 

2. There is a pyorrhetic condition at the gum margin, though no 
particular pus flow is noted. The gums are often flabby and the teeth 
usually isolated and overstrained; later an abscess develops on the 
lateral aspect at a point a little higher up toward the apex, usually 
at the gingival third. There may be no detectable connection between 
the two, but probably a deeper infection has occurred, the avenue 
being along the connective-tissue spaces, the bloodvessels or the glands 
of Black. Hartzell and Henrici claim to have found Streptococci 
viridans deep in pericemental tissue (see page 654) . In one case of this 
sort the fistula was formed over the highest point of the middle 
third of the root of a cuspid retained for plate work. The gum 
margin was flabby, but not markedly pyorrhetic. There was firm 
tissue at the bottom of the space on all sides. The pulp was vital. 
Examination showed a small calculus on the root surface below the 
fistula. The abscess tract was limited. Sometimes it is of greater 
extent. Fig. 640 will illustrate how this occurs. 

3. An acute swelling occurs over a root, the gum margin is un- 
broken, a discharge of glairy or purulent material occurs, and a 
calculus or none may be found. In this connection Fig. 233 shows 
that a calculus may exist as a primary cause of the pericemental 
abscess. As calculi of gouty (sodium bi-urate) or other origin occur 
in other parts of the body and in the pulp, there is no valid reason 
why one should not occur in the pericementum or upon the root 
under it if some sluggish condition of the circulation renders the 
tissues into a degenerative state favoring it. (See page 62.) The 
pericementum contains white fibrous tissue which is particularly 
prone to such deposits. 

Whether such a deposit occurred primarily in the case of the cuspid 
described under Class 2 and infection followed, or whether the infec- 
tion and pus came first and the calculus followed is not quite clear. 
In two distinct cases, with healthy gum margins, the editor has 
seen an acute circumscribed swelling which was not yet open as a 
fistula and, which was perforated by an explorer, disclosing a loss 
of alveolar bone and a small cavity filled with clear liquid in the 
tissues. The explorer reached the root without obstruction, and 
no calculus was present. After discharge and curettement the 
cavities healed. These two swellings looked like blisters or simple 
cystic swellings near the gum margin. If they had discharged at 
the gum margin they might have produced a gum pocket simulating 
pyorrhea. The theory of a granulomatous formation has been sug- 
gested. As this may lead to cyst formation in apical granuloma it 
is a reasonable hypothesis though the two cases above did not con- 
tain proliferated tissue, some of the cases, however, appear as though 
such a tissue had been previously formed. 



700 



PERICEMENTAL ABSCESS 



Fig. 678 



111 another case a right upper bicuspid was in non-occlusion, pyor- 
rhea had been apparently cured upon the distal and the gum was 
receded for a quarter inch. A year or two later acute pain super- 
vened; there was no evidence of swelling, but a soft spot was found on 
the gum surface over the absorbed alveolar process about one-third 
inch from the tooth. It was opened and a sinus with no evident pus 
thus established to a point perhaps a quarter inch above the resorbed 
gum margin. It has been healed for a year, at this writing. 

4. In some cases of apical abscess the infection may travel along 
the pericementum and develop a secondary abscess at some point 
in the pericementum (as, for example, the bifurcation), as a perice- 
mental abscess. This form corresponds to the cases of Class 2, but 
is apt to be more acute. It is also quite rare. The pulp is, of course, 
dead, at least partially in such a case. 

The subject of pericemental abscess is in some confusion because 
writers have described all these varying phases as pericemental 

abscess, which indeed they are, 
yet they require differentiation 
into : 

1. Cases occurring as a sequel 
to a distinct pyorrhea alveolaris, 
Class 1. 

2. Casesa ssociated with margi- 
nal pyorrhea cases but distant to 
them, in all probability having a 
source of infection in the pyorrhea 
pockets, Class 2. 

3. Cases beginning on their own 
account; the relation of the cal- 
culus if present as a cause or re- 
sult being in doubt, Class 3 (Figs. 
679 and 680). 

4. Cases beginning in an apical 
abscess infection or similarly on a 
perforation, travelling via the peri- 
cementum to another portion of 
the pericementum, Class 4. 

Garrod found crystals of urates in the serum of blisters in gouty 
patients. In gouty patients they are found in joints, and they con- 
stitute the common tophus. (See page 62.) "Urates of sodium are 
also discharged through the skin in gouty abscesses, either in liquid 
or solid form, and with or without pus." (Musser.) Musser 1 states 




Tophi of gout. (Ziegler.) 



Medical Diagnosis. 



PERICEMENTAL ABSCESS 



701 



that a number of these abscesses may discharge without impair- 
ment of the general health or even with benefit to the system. 

Calculi scraped from the roots, in pericemental abscesses exhibit 
in a varying degree a response to the murexid test, the test for 
urates. (Peirce.) The reaction may be very faint in some cases, 
being overshadowed by the calcium phosphate which makes up the 
bulk of these masses; in others it is pronounced — i. e., urates made 
up a portion of the deposits. 

Black 1 by test found urates in nearly all concretions, salivary and 
serumal, about the teeth. While he claimed that this proved that 
urates have no causal relation to pyorrhea, the findings seem rather 
to point to frequent presence of urates in the salivary and serumal 
excretions, which may really be a cause of irritation even when no 
obvious symptoms of gout are present. 



Fig. 679 



Fig. 680 





A and C, vital pericementum; B, gouty cal- 
culus; D, a subgingival calculus. 



A, calculus in area of necrosis 
B, and C, vital pericementum. 



Miller's demonstration of a calculus upon an unerupted tooth is 
to be recalled. It seems fairly reasonable, therefore, to suppose 
that in rare cases such a calculus may be the result of either gout 
or a local degeneration and act as an exciting cause. 

Morbid Anatomy. — Aside from the state of the teeth which show 
evidences of a tendency to secondary dentin and nodule formation, 
it has been noted that the abscess is intrapericemental, not sub- 
pericemental. Figs. 681 and 682 show the inflammatory swelling of 
the pericementum ; the central abscess cavity, and the loss by resorp- 
tion of the alveolar process may easily be calculated. The original 
chronic nature of the local irritation in this case is evidenced by 
the presence of hypercementosis. The case in Fig. 681 suggests a 
granuloma. 



» Dental Review, 1894. 



702 



PERICEMENTAL ABSCESS 



Symptoms. — These have been largely foreshadowed in the dis- 
cussion of the pathology. Upon some tooth, often a vital tooth, there 
appears an uneasiness, at first not very painful, followed later by an 



Fig. 681 




Two views of an intrapericemental abscess. Pulp vital. (Kirk.) 
Fig. 682 




Transverse section through buccal roots and pericemental abscess shown in Fig. 
681, showing intrapericemental abscess cavity with fistulous outlet and nearby areas 
of nodular hypercementosis, (Kirk.) 



PERICEMENTAL ABSCESS 703 

inflammatory swelling which may produce acute pain and then dis- 
charge a glairy fluid or purulent matter. There is an absence of 
the marked phlegmonous inflammatory involvement of contiguous 
tissues common in cases of acute apical abscess. The fistula may 
persist after the discharge and the case may first be seen in this con- 
dition. If it discharges at the gum margin it establishes an ordinary 
pyorrhea. 

Fig. 683 




Pericemental abscess. (Talbot.) (Photograph by Latham.) 

D. D. Smith calls attention to the absence of marked pain upon 
tapping and the production of a feeling of apprehension upon the 
part of the patient during the stages preceding the formation of the 
fistula. In other cases the shifting of the tooth from its position is 
the first noticeable symptom, followed later by the pain, and later 
still by the discovery of a pocket alongside the tooth. 

Diagnosis. — In making the diagnosis the symptoms described are 
to be borne in mind, but the disease may be confounded with several 
diseases having somewhat similar symptoms. An acute apical 
abscess due to gangrenous pulp may be differentiated by obtaining 
evidences of pulp death, previous root-canal treatment, etc. There 
is also much greater pain upon percussion than in pericemental 



704 PERICEMENTAL ABSCESS 

abscess. If slowly and painlessly formed it may be still more con- 
fusing, but the pulp is dead. 

If the apical abscess be in the third stage it may be differentiated, 
if any doubt exist, by incision and subsequent exploration. 

An acute lateral abscess due to a root perforation is more difficult 
of differential diagnosis, but after incision evidences of perforation 
may be sought externally, or the root canal may be opened. In 
these acute conditions the .T-ray may render valuable aid. Trans- 
illumination of the alveolar process with a powerful electric mouth or 
antral lamp may demonstrate a more deeply colored area. The pulp 
being found alive by any reliable test is evidence that the case is not 
apical abscess and probably pericemental abscess. In a few cases of 
partial gangrene of the pulp the pulp may test as vital, yet really the 
symptoms be due to apical abscess. 

Treatment. — If the pericemental abscess 
Fig. 684 discharge by way of the gum margin, infec- 

tion from the oral cavity occurs and the 
pocket originally formed becomes deeper. 
The case simulates then a pyorrhea alveolaris 
beginning at the gum margin. The treatment 
is then conducted accordingly. If the swell- 
ing occur upon the gum, at a point more of 
less midway upon the root, or if transillumi- 
nation demonstrates a deep inflamed spot and 
A, calculus. the pain warrant, it should be opened under 

antiseptic precautions. A semicircular flap may 
be raised, or a simple incision made preferably under local anesthesia 
in some form. The diseased area should be explored for calculus and, 
whether found or not, the necrotic tissue should be curetted away. 
Next, the pocket should be syringed out with an antiseptic and filled 
with balsam of Peru or a clot induced. The flap is next laid into 
place. The mouth should be kept in an aseptic condition during the 
healing of the parts. It is well to have the patient keep the sinus 
open with a needle to ensure healing from the bottom rather than 
ballooning by pus, which may cause recurrences. The systemic 
considerations are the same as those described for pyorrhoea. 

The cases are sometimes annoyingly recurrent and in case of 
isolated teeth the overstrain may render them incurable. Those 
cases in which the pocket is associated with a groove between 
buccal roots of upper molars with which a crevice between roots 
exists are practically hopeless, as there is persistent inaccessible 
infection. 




CHAPTER XXIII. 
REFLEX NEUROSES. 

Reflex neuroses consist of (1) pain produced in parts distant 
to the point at which irritation is produced, while pain may or 
may not be absent at that point (sensory reflexes), or (2) they may 
consist of muscular excitation in parts distant to the cause (motor 
reflexes), or (3) they may consist of nutritive disturbances in the 
distant part, probably a form of motor reflex in which the trophic 
nerves or the vasomotor nerves are reflexly irritated so as to 
produce trophic disturbances. 

The source of irritation may be in the dentinal fibril, in the pulp, 
or in the pericementum, producing sensory or motor or trophic 
reflexes in other parts or the source of irritation may be in some 
other location than about the teeth and produce phenomena about 
the face or teeth. 

Whether of dental origin or not a sensory reflex is called neu- 
ralgia, though the cause of a neuralgia may possibly be a direct 
irritation of a nerve trunk or terminal. 

While all reflex dental disturbances are, as a rule, located in some 
part of the great nerve branch supplying the source of irritation, 
the irritation may be reflected to distant parts; first, of the same 
cranial nerve, and secondly, to other nerves. That is, pain having 
its origin in one of the upper teeth is most likely to be referred to 
a point or points in the distribution of the superior maxillary divi- 
sion of the fifth nerve. Disturbances in or about the lower teeth 
are usually referred to the distribution of the inferior maxillary 
division. In affections of either upper or lower teeth the pain may 
be referred to the ophthalmic division. In all of these cases, but 
most notably in connection with disturbances of the upper teeth, 
the usual symptom of trifacial neuralgia — tenderness of the supra- 
orbital and infraorbital nerves at their points of emergence upon 
the face, the supraorbital and infraorbital foramina — is commonly 
present. A reflex may be multiple, that is, to several points at once 
e. g., in one case the sensations were felt in the ear, temple, mastoid 
region and about a molar- tooth. The cause was apparently a small, 
"headless boil" in the external auditory meatus. 

The writer believes that to some extent all the varieties as above 
43 (705) 



706 REFLEX NEUROSES 

defined are to an extent commingled inasmuch as a persistent sensory 
reflex to some locality results in tenderness of the spot, showing a 
hyperemia due to a vasomotor reflex via the sympathetic system 
and therefore a trophic reflex. 

Cases are extremely rare where the reflex pain is referred to the 
opposite side; so unusual is this occurrence that its mention 
warrants suspicion that other sources of irritation exist upon the 
side referred to. 

The extent of acuteness of reflex pain bears no direct relation to 
the apparent extent of the source of irritation. 

As might be surmised from the function of the dental pulp, painful 
reflex dental disorders are more common in connection with diseases 
of the pulp than with those of the pericementum. 

In diseases of the eye the reflexes are usually referred to branches 
of the ophthalmic division. 

REFLEX NEURALGIA FROM EXPOSED DENTIN. 

The exposure of the dentin to external sources of irritation is 
followed by reactions governed, first, by the degree of sensitivity 
inherent in the protoplasm of the tissue; and secondly, by the degree 
of hypersensitivity induced in it. Reflex disturbance due to these 
irritations is more common in the class of persons called "neural- 
gics," L e., in those whose nervous irritability is exalted, a condi- 
tion which may remain even in nervous exhaustion. Like direct 
pulp pains, unless actual pressure be exerted upon the affected 
tissue, there is no localized pain. In the absence of deliberate irri- 
tation, the pain may be referred to any portion of the peripheral 
distribution of the fifth nerve upon the face, but if an acid liquid, 
such as lemon juice or vinegar, or sugars be taken into the mouth, 
pain is excited, which is referred indefinitely to the teeth of one side, 
frequently of one jaw. Reflex pains due to this cause often appear 
when there is but little loss of dentin. 

When carious cavities have proceeded to any depth evidences of 
direct pulp disturbance are obtained through the increased response 
to thermal changes. 

Reflex pains from exposed dentin appear most commonly in con- 
nection with exposures at the neck of the tooth and upon abraded 
areas. Obstinate and persistent neuralgia, positively referred to 
another nerve branch, may apparently owe its origin to so slight a 
cause as exposure at the neck of a tooth of a line of dentin (Fig. 686). 
The proof of the connection between the two is made clear by a 
disappearance of the neuralgia after the exposed dentin has been 




Fig. 685.-Plan of the fifth cranial nerve, showing the relationships of the dental 
nerves. (After Flowers.) 




708 REFLEX NEUROSES 

subjected to the action of powerful caustics (especially silver nitrate), 
destroying the dentinal filaments to some depth. The connection 
between the two may be revealed only by accident; the contact of 
a toothpick, a dental instrument, or the finger-nail may induce a 

paroxysm of pain. In one case, 
FlG - 686 after removal of calculus, the 

necks of the lower incisors be- 
came a cause of severe neuralgia, 
compelling the use of silver ni- 
trate. 

While in some cases the dental 
origin of reflex pain may be made 

Sites of dentin exposure frequently asso- ° , . , . „ . 

dated with reflex pains. clear by the induction or a painful 

. response in the area of reflection, 
by irritating a tooth pulp, this reaction is not constant. The causal 
relation is only certain when the cure of localized dental disease 
is followed by a disappearance of the neuralgia without further 
treatment. This proof should be exacted in all cases. 

REFLEX NEURALGIAS FROM PULP DISEASES. 

The disturbances require classification according to the distance 
between their source and their manifestations. 

In the Fifth Pair of Nerves. — In neuralgic patients any variety 
of pulp disease may cause comparatively distant pains. But, as 
Black has pointed out, 1 the general rule is, that the more chronic and 
profound degenerative diseases of the pulp are much more liable to 
give rise to distant reflex pains than are acute pulp diseases. 

The pains of acute hyperemia and of acute inflammation of the 
pulp are usually referred to the region of the tooth affected, or to a 
corresponding nerve trunk. In conditions of nodular calcifications, 
chronic inflammation, and pulp degenerations, the source of the reflex 
pains is all the more obscure from the fact that in these chronic 
degenerations direct dental symptoms may be entirely absent, and 
are only elicited upon the most searching examination and exhaustive 
tests. In some cases of pulpitis even removal of the pulp by cocain 
has been followed by a neuralgia due to irritation of the nerve trunk 
in the pulp stump at the apex, so proved by cure through strong 
sedatives applied via the canal. In one case the neuritis lasted 
several days. 

There is no constancy in the location of the pain due to any of 

1 American System of Dentistry, vol. i. 




REFLEX NEURALGIA FROM EXPOSED DENTIN 709 

these causes; but pain in or about the eye, supraorbital foramen, 
infraorbital foramen, side of the nose, the temporal and anterior 
auricular region, in the ear, down the side of the neck, in the mastoid 
region, even to the shoulder, the arm and about the heart. The pains 
may be acute and lancinating or merely of a mild nature or possibly 
the condition of localized "tenderness" may develop. Many of these 
cases receive attention from the general 
practitioner, and the painful attacks re- FlG - 687 

curring at irregular intervals are relieved 
by analgesic remedies — phenacetin, acet- 
anilid, exalgin, etc. — and no attention 
paid to a probable dental source of the 
disorder. It should be a routine practice 
to examine the teeth in cases presenting 
pains of the type and in the situations 
described. Acute diseases of the pulp, 
including suppuration, notably abscess 
of the pulp, usually have attention di- 
rected to the teeth through pain induced 

, , . . . Spots of tenderness in reflex 

by thermal Changes, SO that their diag- neuralgias of dental origin. 

nosis is quickly made. Not so, however, 

with the chronic degenerative changes, except possibly of pulp 
nodules ; for if the pulp is in the late stages of degeneration, it may 
require repeated applications of cold and heat to elicit a response 
from teeth which do not respond by tenderness upon percussion. 

Failing to obtain evidence of pulp disorders, examination should 
be made for exposed and hypersensitive dentin. Then, examination 
of the pericemental reaction of each tooth should be made, and for 
any evidences about the teeth pointing to pericemental disturbance. 
(See page 483.) 

Lauder Brunton 1 records that, in his own case, temporal neuralgia 
accompanied by tender eyeball was found due to exposed dentin 
upon the posterior cervical surface of a lower third molar (see Fig. 
686) . The same writer 2 announces that " so frequently are headaches 
dependent upon decayed teeth, that in all cases of headache the 
first thing I do is to carefully examine the teeth;" as should every- 
one else. Upson cites by radiograph a case of severe headaches of 
years standing, cured by extraction of an impacted cuspid. 3 Brunton 
explains the painful reaction upon the accepted hypothesis of the 
pathology of megrim, that it is due to spasmodic contraction of the 

1 St. Bartholomew's Hosp. Rep., vol. xix. Reprinted in his Disorders of Digestion. 

2 Ibid. 

3 Raper, Items of Interest, August, 1912, p. 575. 



710 REFLEX NEUROSES 

peripheral end of an artery, with dilatation of the proximal portion. 
"Irritation in the tooth is reflected to the cervical sympathetic 
ganglia and causes spasmodic contraction of the arteries through 
irregular stimulation of the vasomotor nerves." 

An abnormal tooth located in the anterior floor of the nasal cavity 
was the cause of headache for years, so proved by cessation of head- 
ache after its surgical removal. When sepsis is present one must 
differentiate between reflex neurosis as above and a possible trans- 
ference of infection from foci of infection, as various cases of iritis, 
headache, etc., have been due to apical granuloma, pyorrhea, etc. (see 
pages 561 and 694) and may possibly be due to septic living pulp 
The cerebral, intestinal and other symptoms arising in pathological 
first dentition are mainly referable to pulp disturbance (see page 
70) and reflexes arising therefrom. 



REFLEX PAINS FROM DISEASES OF THE PERICEMENTUM. 

As a general rule, pericemental pains are located at the affected 
tooth; but in some of the disorders the teeth may not be tender upon 
percussion, and yet excite reflex pains in other parts, the proof of 
the connection being determined by a disappearance of the pain 
upon extraction of the tooth. The roots in such cases usually present 
either a hypercementosis or show that resorption of a portion — it 
may be a major portion — of the root has occurred. 

In cases of hypercementosis it is assumed that the source of the 
irritation is pressure upon the nerves of the pericementum by the 
hypertrophic growth. Very widespread disorders may arise from 
this source. 

Flagg 1 records many varieties of trifacial neuralgia; pains in remote 
parts of the body; grave functional disorders of the eye and ear; 
and motor disturbances — chorea, epilepsy, and paralysis — having a 
direct demonstrable connection with hypercementosis. Insanity has 
also been produced. 

He mentions violent attacks of trifacial neuralgia as the most 
common reflex disturbance from this source; and next, long-continued 
pains in the ear or eye of the affected side. The existence of acute 
disease of these organs is usually diagnosed by the general practi- 
tioner. He states that aural and ocular disturbances, both functional 
and painful, are of gradually increasing severity. 

In examining for a dental source of such pains, exposed dentin, 

1 Dental Cosmos, 1878. 



REFLEX PAINS FROM DISEASES OF THE PERICEMENTUM 711 

pulp diseases, and inflammatory affections of the pericementum 
should be first excluded. In examinations by percussion a different 
response may be obtained from some one tooth than from the others. 
Hypercementosis of a particular tooth may be suspected if finding 
the gum line slightly receded and the tooth attachment unusually 
firm; if, in addition, vague gnawing, heavy dental pains have persisted 
at intervals over a long period, the diagnosis is probable. It is only 
certain when tapping upon the tooth brings on a paroxysm of 
neuralgia, or a radiograph actually exhibits the hypertrophic 
growth. The remedy is extraction. Any root fragment left unex- 
tracted may perpetuate the reflex disorder. The writer has recently 
treated a case of neuralgia due to a lingual root of a left upper first 
bicuspid which was retained in the gum after extraction. The gum 
had healed perfectly over it. It was only discovered by the use of 
the arrays. 

Painful affections referred to the neighboring region of the affected 
tooth, or diffused through the distribution of the corresponding 
nerve trunk, or to the eye or ear, may accompany the process of 
resorption of the roots of permanent teeth. Gillman 1 records a case 
where facial paralysis disappeared upon extraction of a tooth which 
had long been the seat of disturbance and which, upon extraction, 
revealed resorption of its root. In these obscure cases a radiograph, 
if taken at once, will be a great .aid in the exclusion or diagnosis of 
pericemental and root abnormalities. 

All of the acute or chronic, septic or non-septic, inflammations of 
the pericementum may give rise to reflex pains. The most common 
causes of the reflex pains are found in that stage of pericemental 
irritation which antedates acute septic apical pericementitis, prob- 
ably a granuloma. Unless an exacerbation of the reflex disorder, 
or symptoms referable to that region, be induced by pressure or per- 
cussion on the tooth, a causal relationship is only made out by either 
relieving an existing dental disorder (for example, finding and curing 
an incipient apical abscess due to moist gangrene), a radiograph for 
granuloma, or extracting the teeth. 

Cases of ovarian and uterine neuralgia and sciatica and cases of 
obstinate pains in the knee, toes, and fingers have been traced to 
dental irritation of some one of the varieties named, the proof of 
association being disappearance of the pain with loss of the tooth. 
Here the probable connection is focal infection rather than a reflex 
neurosis. 

1 Boston Medical and Surgical Journal, 1867. 



712 REFLEX NEUROSES 

IMPACTED TEETH AS A CAUSE OF NEURALGIA. 

Neuralgia of varying degrees of severity is a common accompani- 
ment of impacted teeth. It is most frequently noted in connection 
with eruption of the lower third molars, not only because this tooth 
is the one most frequently impacted, but because of the anatomical 
relations of its roots with the inferior dental nerve. 

In the milder forms of impaction, those in which eruption, though 
delayed, is subsequently completed, the pains, are commonly local- 
ized and associated with but occasional attacks of rigidity of the 
masseter muscles. If, however, the crown present horizontally or 
nearly so, and its progress is arrested by impaction against the 
posterior w r all of the lower molar, or if its progress be arrested by 
permanent imprisonment of the advancing crown between the pos- 
terior surface of the second molar and the base of the coronoid 
process, not only may intense local pains be induced, but severe 
reflex disturbances of both a sensory and motor character may occur. 
In some of these cases root formation is completed, although the 
crown of the tooth does not advance, in which case compression of 
the inferior dental canal and its contents may occur and cause grave 
reflex disturbances. The local irritation about the root, due to root 
growth, may excite continued constructive action by the peri- 
cementum, and the hypertrophic growth in its turn may be the 
source of reflex neuralgias. 

Complete imprisonment of the entire tooth has been found to be 
the exciting cause of facial neuralgias, for the cure of which extensive 
surgical operations have been performed. 

Impacted cuspids and other teeth may excite no other symp- 
toms than reflex neuralgia. The possible connection between an 
impacted tooth and neuralgia is made out after excluding other 
dental causes, when it may be observed that one or more of the 
permanent teeth are absent from the dental arch, at dates long after 
their normal time of eruption. 

A condition equivalent to partial impaction, in which dental irri- 
tation may be the source of reflex neuralgia, is seen when the teeth 
are crowded into arches too small for their accommodation. During 
the period of eruption severe maxillary pains may recur at intervals. 
The diagnosis is by means of the z-rays. The production of insanity 
as a reflex condition has been discussed on page 128. 

PHANTOM ODONTALGIA. 

This is a form of neuralgia in which symptoms similar to tooth- 
ache appear in the edentulous jaws or in locations from which teeth 



PHANTOM ODONTALGIA 



713 



have been extracted. The name was applied by J. Foster Flagg. 
It seems to be due to the compression of nerve-endings by dense 
bone. It may, of course, be a reflex neurosis from some other focus 
of pulp or pericemental or nerve trunk irritation. Attention has been 
called to a possible latent focal infection left upon extraction, a granu- 
loma not having been removed. This would be found by the surgeon 
as a cavity rather than a dense bony whorl. 

Fig. 688 




The arrow points to a dark, three-sided shadow — a bone "whorl." The X on the 
shadow is caused by a scratch on the negative. (Radiograph by Pancoast. Courtesy 
of H. R. Raper.) 



Any history obtainable of a previous local inflammation should 
be obtained, and if the pain is localized in any spot the bony tissue 
may be broken Up by operation with a view to removal of such a 



714 REFLEX NEUROSES 

cicatricial inclusion of nerve terminals. At least in troublesome 
cases such a simple operation is admissible. Oyer reports successful 
operations for removal of "bone whorls," the cause of neuralgia 
(see Fig. 688). 

PARALYSIS OF THE SENSORY TRACTS. 

The operation of extraction and occasionally disease of the pulp 
and pericementum have produced a temporary paralysis of a branch 
of the fifth pair and loss of sensation in the lip or cheek may result. 
So far as observed the cases are of not more than a few months' 
duration and may be ameliorated by massage, either passive or 
vibratory or by faradization. 

MOTOR DISTURBANCES FROM DENTAL DISEASES. 

Motor disturbances due to dental irritation may occur as recurrent 
or persistent contraction or paralysis of muscles, together with more 
or less chorea; in rare instances epilepsy and hystero-epilepsy. 
Twitching of muscles of the affected side of the face, ranging from 
slight affection of the occipitofrontalis or orbicularis palpebrarum 
to recurring spasm of the elevators and depressors of the lower lip, 
are far from uncommon phenomena attendant upon pulp and peri- 
cemental diseases. In one case mentioned by Guilford 1 a pulp 
nodule was the cause of tic douloureux (painful muscular contrac- 
tions) of two years' standing. Varney Barnes cites a case of " blinking 
of the eyes," caused by an impacted tooth. 2 A case of recurrent 
epileptic attacks was proven due to a tooth brush bristle forced into 
the gum. 3 

Contraction of the masseter muscle is a common accompaniment 
of retarded eruption of the lower third molar, which may be inten- 
sified until the condition is fitly termed trismus, in some cases of 
partial impaction of the teeth. Partial trismus has been found due 
to a general overcrowding of the dental arch. 4 Records of cases of 
torticollis, due to dental diseases, are also given by Brubaker, under- 
stood now as probably due to focal infection and as of rheumatic 
character. 

Cases of facial paralysis, and cases of paralysis of one arm, of 
paraplegia and hemiplegia, and even of general paralysis, have been 
noted as disappearing after the extraction of diseased teeth. It is 

1 Private communication. l Raper, Items of Interest, August, 1912, p. 575. 

8 Dental Cosmos, 1910, p. 594. 

4 Brubaker, American System of Dentistry. 



MOTOR DISTURBANCES FROM DENTAL DISEASES 715 

noteworthy that in these cases, as well as in several cases of tetanus 
recorded, the probability of an infection entered into the patho- 
genesis of the nervous diseases. 

Stellwagen 1 records a case where symptoms of partial hemiplegia 
followed upon the operation of capping the pulps of two molar teeth; 
the symptoms disappeared promptly upon extraction of these teeth. 
A case of facial paralysis followed extraction of seven roots upon one 
side. It was successfully treated by eight applications of a weak 
galvanic current. 2 Facial paralysis has also followed the eruption 
of teeth, as of a second molar. Infantile paralysis has also been 
caused by dentition (see page 75). 

Cases of insanity arising from dental diseases have been recorded; 
they were both maniacal and melancholic. In several of them a 
restoration to a normal mental state followed promptly upon removal 
of the offending teeth. In some of these cases a preexisting maxillary 
neuralgia directed attention to the teeth as possible sources of the 
nervous diseases. 

Dr. E. Ballard Lodge 3 reports a case from the practices of Drs. 
Upson and Stephan in which a lady had suffered from acute melan- 
cholia and insomnia. A radiograph revealed an impacted upper 
third molar pressing against the distal side of the second molar. 
Extraction effected a cure. Upson 4 reports a number of like cases, 
as well as some due to pulp and pericemental disease. The local 
conditions were painless. 

Cases of deafness have been recorded due to diseases of both pulp 
and pericementum, notably to hypercementosis. Deafness which 
has persisted for a long period has been markedly lessened by the 
extraction of teeth the seat of disease. Cases of suppurative otitis 
media have been regarded as having pathological association with 
septic diseases about the teeth, from the fact that the aural trouble 
subsided immediately after extraction of the diseased teeth (prob- 
ably due to focal infection). 

Sensory disturbances of the eye, associated with dental diseases, 
have been alluded to; in addition to these, grave structural and 
functional diseases of the eye, traceable to dental causes, have been 
recorded, such as motor and trophic disorders. 8 Among the latter 
may be mentioned corneal inflammation and ulceration and phlyc- 
tenular conjunctivitis. These are probably due in part to reflex 
trophic disturbances, but possibly to focal infection. 

1 Private communication. 2 Griefswald: Cosmos, 1906. p. 356. 

• Dental Summary, 1908. * Dental Cosmos, 1910, p. 526. 

6 See Brubaker, American System of Dentistry, vol. iii, for very full and detailed 
discussion of these subjects. 



716 REFLEX NEUROSES 

Irregular paralyses of the third, fourth, and sixth nerves of the 
affected side have been noted. 

Amblyopia and functional blindness without retinal conditions 
to account for it have been found to arise from notably advanced 
degenerative changes in the dental pulp, sight returning to the eye 
after loss of a diseased tooth. DeWitt 1 records a most instructive 
case where temporary blindness was associated with septic apical 
pericementitis, disappearing after evacuation of the abscess and 
reappearing when secondary inflammatory action arose in the peri- 
cementum. The ocular affection disappeared permanently and almost 
entirely with the loss of the tooth. Whether this was a neurosis or a 
focal infection is in doubt. The history of this case illustrates the 
important causal relationship of reflex disturbances with late pulp 
degenerations, for the blindness arose two months after some teeth 
were filled, and existed for twelve years before the septic apical 
pericementitis appeared. (In this case probably a granuloma was 
the intermediate condition.) 

Trophic Disturbances Following Dental Diseases. — Two eases of 
localized alopecia (loss of hair) have been reported, 2 obstinate during 
the dental disease and cured by the cure of a pulpitis in one case 
and extraction of a root for suppurative pericementitis in the other. 
Such cases show a vasomotor disturbance in the distant part. Infec- 
tion transference from a septic living pulp is claimed by Price. 3 

DENTAL PAIN ARISING FROM OTHER THAN DENTAL SOURCES 

Conditions of pain the reverse of those discussed — i. e., pain 
definitely or indefinitely located in teeth which exhibit no morbid 
conditions whatever — demand occasional attention at the hands of 
the dentist. 

Chronic malarial poisoning, as stated in the beginning of this 
chapter, may give rise to periodical attacks of maxillary neuralgia. 
As in the gouty cases, the constitutional cause of the disturbance is 
made clear through the therapeusis most effective, viz., the periodical 
recurrence of the pain leads to the inference of a malarial origin, and 
to the administration of quinin. Anemia and other conditions in 
which there is accumulation of products of metabolism also cause it. 

Syphilitic pains in the jaws have a pericemental character, and 
other evidences of syphilis are present which point to a diagnosis. 

Pains in or about the teeth are occasional accompaniments of 

1 Quoted by Brunton, Disorders of Digestion. 

2 Mounier: Le Laboratoire, 1907. 

3 Lecture on Focal Infections, Pennsylvania State Dental Society, 1917. 



DENTAL PAIN FROM OTHER THAN DENTAL SOURCES 111 

diseases of the brain or its vessels, and of pregnancy or diseases of 
the uterus, kidneys, and bladder. 

Disease in any portion of the fifth cranial nerve may cause pain 
referred to the teeth, for example, inflammation of the nerve trunk, 
a tumor in the nerve,. or a tumor pressing upon the nerve trunk, 
or a portion of fractured bone so pressing, or a cicatrix contracting 
upon a nerve. 

Dental pain during pregnancy, without any direct evidence of 
dental disease, is relatively common. 

Disorders of the lower bowels, causing constipation, may give rise 
to pain referred to one or more teeth, the pain ceasing promptly 
upon the administration of an active evacuant. 

Influenza occasionally produces antral empyema or neuralgia about 
the dental region as one of its sequelae. 

Pain may appear in one or more teeth either with or without 
association with pain about the maxillae or tenderness at the foramina 
of emergence. If there be possible causes in defective teeth or teeth 
with fillings in which pulp irritation is a possibility, there may be 
difficulty of diagnosis. There may be a history of an attack of 
influenza or even of coryza, with the common variety of which 
dental pains are often associated. Abscess in the maxillary sinus 
or other sinuses may do the same. 

It may occur after influenza has seemed to have disappeared. The 
pain is at first generalized over the entire head, but gradually local- 
ized in one or several upper teeth, more frequently in the second 
molar, occasionally the bicuspids. It sometimes is so severe that 
the patient thinks an abscess is forming. 

There is almost always pain in the molar region when pressure is 
made upon the inner alveolar portion of the hard palate, and sensi- 
tivity of the external alveolar region. 

For the pseudoodontalgia Roy recommends a capsule containing 
the following: 

1$ — Antipyrin gr. vij 

Quinine hydrobromid gr. iij 

Sodium bicarbonate gr. iij 

Sig. — One dose. Increase and prescribe four times a day. 

Locally he recommends: 

1$ — Mentholis gr. x 

Acidi borici 3iij 

Vaselini 5j — M. 

Sig. — A small portion to be applied within the nostrils on rising and retiring. 

Treatment of Facial Neuralgia. — The cause should be sought for, 
and, if possible, removed. If due to disease of the teeth, these should 



718 REFLEX NEUROSES 

be relieved; if due to eye disease, or other cause, this should receive 
attention. Should one not discover the cause, yet desire to afford 
a relief pending its discovery, the accepted remedies antipyrin, 
acetanilid, and phenacetin, combined with caffein or the bromids, 
are useful. 

1$ — Antipyrini (vel phenacetini vel acetanilidi) . . 3J 

Caffeinae citratis gr. x 

Potassi bromidi 3iij — M. 

Ft. in chart No. x. 

Sig. — One every thirty minutes until relieved. (Hare.) 

If the patient be constipated, the bowel should be freed of toxic 
substances by the use of castor oil, repeated as necessary. Castor 
oil in small doses is antineuralgic. 

In obstinate neuralgia and other painful affections with unremov- 
able cause, the application of the x-rays has been urged by Morton 
as highly efficacious in relieving pain, often for a considerable time. 
The blue ray is also used. A remedy of exceedingly simple nature 
was introduced by Verge and Pitres in 1902. It consists of injecting 
into the mucous membrane or skin, about where the pain seems to 
originate, 1 c.c. of alcohol (85 per cent, plus 1 per cent, cocain is 
preferred by Lenson) at the temperature of 60° C. by means of a 
hypodermic syringe. Asepsis must be provided for. 

A slight humming sensation and swelling of tissue occurs about the 
area of injection. The pain disappears for a long period after one 
or two injections a week apart. 

Dr. H. I. Patrick 1 recommends the injection in trifacial neuralgia 
not dependent upon recognizable conditions as preferable in the 
middle aged and aged to the Gasserian operation, and sets forth 
the landmarks as well as the conditions for the operation. 

The Gasserian ganglion has also been injected with alcohol with 
apparent satisfaction, and is less serious than radical operation. 

A deep injection into the nerve trunks has high medical indorse- 
ment. A case in which the face became black on the side of injec- 
tion was also followed by relief and subsidence of the congestion. 
The method has been objected to by some. It has been recorded 
that myosis, and prickly or tingling sensation or paralysis of the part 
or nearby muscles of temporary nature are by-effects. Injection 
of the nerve trunk with dilute osmic acid has been practised by 
surgeons. 

Strychnin in fairly large doses has been employed under medical 
supervision. When the cause cannot be determined the nerve itself 
may be resected. These are measures in the hands of surgeons. 

1 Journal of the American Medical Association, January 20, 1912. 



CHAPTER XXIV. 

INFECTIONS OF AND FROM THE MOUTH. 

Inflammations of various sorts may appear in or about the mouth 
as well as certain symptoms regarded as pathognomonic of certain 
systemic diseases. The dental diseases involving oral inflammations 
are to be so classed, but have been separately described. Here various 
forms of stomatitis not distinctly dental will be dealt with. 



STOMATITIS. 

Definition. — By stomatitis is meant an inflammation of the mucous 
membrane of the mouth. If secretion is markedly increased it may 
be termed catarrhal stomatitis. 

Varieties. — It may be localized, as in marginal gingivitis, or be 
diffuse; and, again, be accompanied by localized tissue destructions — 
ulcerations; the character of the ulceration differs according to its 
probable causes. 

Occurrence. — Most of these diseases belong to the period of child- 
hood, although localized ulcerative stomatitis may appear in the 
adult. 

(Simple. 
Infective 



Catarrhal stomatitis 



Local 



(Fermentations. 
Diphtheria. 
Gonorrhea. 



Symptomatic 



Ulcerative stomatitis 



Local 



Symptomatic 



Eruptive fevers. 
Syphilis. 
Tuberculosis. 
Typhoid fever. 

{Iodids. 
Mercury. 
Lead. 
Pilocarpin, etc. 
Aphthae. 
Thrush. 

Noma and gangrenous stomatitis. 
Herpes. 

Syphilis (primary). 
Gonorrhea. 
Vincent's angina. 
Stomatitis epizootica. 
Actinomycosis. 
Ludwig's angina. 

( Secondary. 
' * \ Tertiary. 
[ Scurvy. 

(719) 



Syphilis 



720 INFECTIONS OF AND FROM THE MOUTH 

Causes. — The causes of stomatitis are so many and varied as to 
suggest a classification under heads according to assignable causes. 
While it is true that bacterial infection has not been shown to be a 
direct cause of all of these conditions, some degree of causal relation- 
ship is probable in all of them. The disease may, however, be 
included under two heads according as they are or are not localized, 
and necrotic. The less localized cases appear as a diffuse catarrhal 
affection, affecting wide areas of the oral mucous membrane; the 
others appear as spots of localized tissue destruction attended by 
surrounding hyperemia. 

Simple Local Catarrhal Stomatitis. — The general symptoms of 
catarrhal inflammation — heat and swelling, with deepened color of 
the mucous membrane, followed by increased secretion and exuda- 
tion — attend several types of oral irritation, such as the irritation 
induced by erupting teeth, particularly of the deciduous teeth. A 
transient eruption may appear in some cases. Inflammation of any 
degree may follow the taking into the mouth of caustic chemical 
substances, such as caustic alkalies, mineral acids, carbolic acid, etc. 
Other irritant drugs and very hot fluids may produce similar results. 
General catarrhal stomatitis is a frequent affection of confirmed 
smokers, and of drinkers of distilled liquors. 

The cure of these conditions consists in the removal or neutrali- 
zation of the cause, and the use of local sedatives and antiseptics to 
allay irritation and prevent infection. The most effective method 
of treating the inflammatory condition is by antiseptic sprays, such 
as diluted Dobell's solution, followed by sprays of strong solutions 
of potassium chlorate. If much pain exist, phenol-sodique is an 
admirable sedative antiseptic, used in 10 to 20 per cent, solution, as 
a spray. A simple stomatitis may be caused by digestive disturbances 
(see below). 

Infective Local Catarrhal Stomatitis. — This in some degree is a 
common, perhaps the necessary, antecedent condition to many of 
the ulcerative forms of stomatitis. It is probable that many of the 
cases of stomatitis found iti infants, children, and adults are due to 
unusual fermentations occurring in the mouth. Children whose 
nursing bottles are not kept clean; those who at a later age suffer 
from neglect of the teeth and from the effects of improper food: 
adults in whose mouths dental disease is widespread, and whose 
oral hygiene is very faulty; all exhibit abnormal conditions of the 
oral mucous membrane — more or less swelling, softness, and deepened 
color of the mucous membrane, a coated tongue, and offensive 
breath, with an increase of oral secretions. 



STOMATITIS 721 

The complexus of oral symptoms is commonly, and also by the 
general practitioner, regarded as symptomatic of gastric, intestinal, 
and hepatic disorders, as doubtless it is, but the causal relation- 
ship is in many cases probably the reverse of that implied in such 
opinions, for it is probable that the disturbances of digestion are 
fermentative in character, and the organisms causing them find their 
way to the stomach from the mouth, which was first affected. The 
treatment of this condition consists in the correction of its causes, 
their non-repetition, and the continued use of oral antiseptics. 

Symptomatic Catarrhal Stomatitis. —Stomatitis in its catarrhal 
form usually accompanies the early and later stages of the eruptive 
fevers, scarlet fever, smallpox, etc. In scarlet fever, smallpox, and 
measles evidences of infection of the oral mucous membrane by way 
of the blood exist and the inflammatory reaction is pronounced. 

Catarrhal stomatitis is one of the manifestations of secondary 
and tertiary syphilis, antedating the appearance of tissue necrosis 
(ulcerations). 

More or less catarrhal stomatitis, confined, it may be, to the 
mucous membrane of the gums, is common in the mouths of phthi- 
sical patients; tubercular ulcers may arise or threaten. In some 
cases the palate has been perforated. Curtis states that these are 
usually fatal. 

The stomatitis of typhoid fever may be regarded as an almost 
essential feature of the disease. 

The effects of drug elimination by the oral tissues have been 
already discussed (see page 568 and 572). 

Mercurials in excess produce gingivitis with puffy gums which 
bleed readily; there is coated tongue, fetid breath in marked cases, 
swollen tongue and cheeks, and exfoliation of the teeth. The history 
of administration of mercurials, and, possibly, of syphilis, as a reason 
for it affords a diagnosis. The mercury should be stopped; atropin 
sulphate, 5 minims of a 1-grain to 1-ounce solution in water, admin- 
istered as an antisialagogue every four to six hours; a 5 per cent, 
potassium chlorate solution in hydrogen dioxid makes a useful 
mouth wash for reducing the local inflammation. 

A case of bismuth poisoning causing ulcerative stomatitis with 
bright blue line on both upper and lower gums is reported by Blight 1 
as cured upon removal of the bismuth dressing. 

Ulcerative Stomatitis. — In all probability these ulcerations are 
always infective. Like catarrhal stomatitis the ulcerative disease may 
have only a local significance or be indicative of some general disease. 

1 British Dental Journal, December 15, 1917, see Dental Cosmos, May, 1918. 
46 



722 INFECTIONS OF AND FROM THE MOUTH 

Ulcerative Stomatitis of Local Significance. — The more usual or 
infantile forms of these disorders are a sequel of catarrhal stomatitis, 
at least of an acquired debility of the oral tissues, and their primary 
cause is, therefore, the cause producing a condition of mucous mem- 
brane which permits the growth of infective organisms. The others, 
aphthae, herpes labialis, and noma, are all probably due to the action 
of organisms. 

Aphthae. — This affection is common in its isolated form, as the 
canker sore. In the catarrhal stomatitis of children, during or after 
dentition, multiple sores frequently make their appearance. The 
condition can best be studied when it appears as an isolated sore in 
the mouth of the adult. The most common situation of the sore is 
at the junction of two mucous surfaces, such as that of the gum with 
the lip or cheek, or that of the floor of the mouth with the gum or 
tongue. Redness diffused over a limited area, followed by a nodular 
hardening, occurs, during which local pain is annoying; the center 
of the hardened area breaks, the epithelium disappearing, forming a 
raw surface, which quickly acquires a rough, yellowish white coating 
which is easily removable. The sores are very painful. 

The mouth is usually otherwise healthy, and there is an absence 
of associated throat and skin affections. 

Occasionally a lymphatic gland is affected. 

The notable fungus is the saccharomyces albicans; this organism, 
when classified by mycologists as a thread fungus, was known as 
the oidium albicans (Fig. 689). The growth of this organism illus- 
trates forcibly the influence of soil on the growth of fungi. It 
does not occur in the mouths of healthy, well-nourished, and clean 
children with good surroundings. It is a disease of childhood, 
particularly of nurslings, and its surroundings is almost always 
confined to bottle-fed babies whose feeding bottles are kept in 
an unclean condition though Brown considers traumatism from 
suckling a cause. Debility of the oral tissues is established in conse- 
quence of the fermentations arising from the source just named, 
furnishing a favorable condition for the development of the sac- 
charomyces (oidium) albicans. The condition produced is known as 
thrush. The infection may be carried from one child to another, and 
if the fungus be brought in contact with an abraded mucous surface 
of an adult it may develop. 

The fungus burrows between the epithelial cells of the mucous 
membrane (Fig. 690), not beyond it. It first appears in small spots 
which coalesce, until large patches of a membranous-like growth 
cover extensive surfaces, spreading by continuity to all of the mucous 
surfaces associated with the mouth, 



STOMATITIS 



723 



As bud fungi flourish only in media of acid reaction, the use of 
alkaline washes is indicated in the treatment of this condition. 
Wiping the patches with dilute phenol-sodique is efficacious. Hy- 



Fig. 689 



Fig. 690 





Saccharomyces albicans, thrush fungus. 
(Miller.) 

drogen dioxid or 25 per cent, iodin 
in glycerin (as Talbot's iodogly- 
cerol) are also useful. Small spots 
may be cauterzed with silver nitrate 
or phenol or trichloracetic acid. 

This condition follows so con- 
stantly upon the taking of very 
indigestible food, such as lobster, 
Welsh rarebit, etc., that acute 
indigestion must be regarded as 
having some causal relationship 
with it. It is also of frequent oc- 
currence in the mouths of dys- 
peptics; that form of gastric dis- 
turbance attended with a deficiency of hydrochloric acid in the gastric 
juice appears to have a constant association with it, though it is prob- 
ably caused by the oidium albicans. 

The appearance of ulcerative stomatitis in children, together with 
its treatment, was discussed in the chapter on Dentition. 

The general treatment of these ulcerations appearing in the mouths 
of children is the administration of a laxative, and the subsequent 
administration of listerine, gtt. x, every two hours. Locally the 
mucous membrane is to be sprayed with hydrogen dioxid, followed 
by sprays of strong solutions of potassium chlorate. 

Localized aphthous patches in the adult are promptly relieved by 
the administration of calomel, gr. ij, at night, followed in the morning 
by a mild saline. The local sore is dried and touched with pure 



Pavement epithelium covered with 
spores of the oidium albicans. (Ch. 
Robin.) 



724 INFECTIONS OF AND FROM THE MOUTH 

carbolic acid. The administration of alkalies before meals, and 
hydrochloric acid after meals, usually remedies the gastric condition, 
unless it be of long standing. A variety of aphthous sore is called, 
from the anatomical situation of the ulcers, follicular stomatitis. 
Irritation and swelling of the mucous follicles in the palatal, 
buccal, and labial mucous membrane are accompanied by more or 
less localized inflammation; the follicles become ulcerous, the small 
ulcers having a uniform size. This condition quickly disappears 
under the treatment advised for ulcerative stomatitis. An indica- 
tion of the bacterial origin of all of these disturbances is seen in 
the efficacy of antiseptics used in their treatment. 

Rubber Sore Mouth. — A form of stomatitis is due to artificial 
dentures resting upon the mucous membrane, and either by pressure 
or light friction, or possibly by preventing radiation of heat, they 
cause desquamation of the epithelium. The part beneath the plate 
assumes a more or less reddened or ulcerated appearance. Vulcanite 
plates that are not smooth upon their surfaces of adaptation may 
produce this physical irritation, but oftentimes such surfaces may 
be covered with infective mucous plaques, so that this may in some 
cases be an added cause. Plates often cause mechanical abrasions at 
the inner part of the margins or actually sink into the tissues. These 
abrasions may, of course, be infected. To prevent this in new plates, 
as is likely and annoying to all concerned, the writer suggests to the 
patient to place a pencil mark on the plate above the point of irrita- 
tion and to remember whether "inside" or "outside," then to scrape 
slightly and repeat as necessary. A good rule in finishing plates is to 
"round" all sharp angles. 

Eilestein has shown that the use of vermillion colored vulcanite 
causes minute pores to appear in the vulcanite which harbors bacteria 
which may induce inflammation of the oral epithelium. 1 The use of 
carmine-colored vulcanite is suggested. The making of smooth con- 
tact surfaces is a duty. 

Treatment. — The treatment consists of rest and healing mouth 
washes. Antiseptics are usually included. (See Gingivitis.) 

Stomatitis Aphthosa Epizootica. 2 — This is the oral expression 
of foot-and-mouth disease occurring in cattle and rarely fatal, and 
usually lasting about eight weeks. The germ is not fully determined 
as yet. It is transferred by contact as to hands of milkmaids from 
herpetic eruptions on the cows or from milk to the mouth. Herpetic 
eruptions and aphthous ulcers are the condition produced. 

1 L'Odontologie. See Deatal Cosmos, February, 1911, p. 248. 
1 Lartschneider: Dental Cosmos, 1908, p. 880. 



STOMATITIS 725 

Equinia (Glanders). — An infectious disease of cattle which may be 
transferred to man, producing a purulent discharge from eyes, nose, 
and mouth. 

Diagnosis. — The diagnosis rests upon the presence of the bacillus 
mallei or the use of mallein as a diagnostic test (Brown) of the disease 
in nearby cattle and the prodromata and later presence of fever, 
pustules on the mucous membranes of the lips, tongue, and some- 
times on the hard palate and throat, occasionally between fingers, 
around nails, or on nipples. These later burst, leaving ulcers with a 
grayish-yellow coating. The pustules dry up without scars in the 
second week. Brown states that it may extend into the system via 
lymphatics and become chronic or even cause multiple abscesses and 
death from toxemia and exhaustion. 

Treatment. — The treatment rests upon antisepsis in so far as the 
local manifestations are concerned. 

Diphtheria. — While the point of first attack of the diphtheria 
bacillus is most marked about the soft palate and tonsils, the false 
membrane forming there and spreading to the pharynx, more or 
less general inflammation of the oral mucous membrane also occurs. 
Hare 1 highly commends aqua hydrogenii dioxidi, in full strength, on 
a swab or 1 to 4 per cent, of water as a spray for the local treatment. 

Gangrenous Stomatitis, Noma, Cancrum Oris. — In ill-fed, ill- 
nourished, and ill-kept cachectic children, or those having had a 
previous debilitating acute infective disease, the debilitation of the 
oral tissues may exceed the grades given, and a disease, probably 
bacterial in origin, may arise which leads to widespread necrosis of 
the cheeks and maxilla?. The condition is called gangrene of the 
mouth, noma, or cancrum oris; the latter term has been applied to 
the less severe varieties. Leukemia is an occasional debilitating cause. 
(Brown.) 

This disease may make its appearance as an ulcer at the junction 
of cheek and gum; in other cases a severe stomatitis arises without 
a primary ulcer. A greater or less extent of the cheek acquires a 
board-like hardness, becoming livid; the overlying mucous mem- 
brane breaks, exhibiting a large slough. The necrosis extends toward 
cheek and jaw, destroying further tissue. The sloughs undergo 
putrefactive decomposition, emitting a stench. The destruction of 
tissue may be arrested, or may proceed, destroying in a few days 
the entire cheek and bony tissues. In the more severe cases the 
disease is almost invariably fatal, because the extent of the tissue 
destruction bears a constant relation to the underlying debility of 

1 Practical Therapeutics. 



726 



INFECTIONS OF AND FROM THE MOUTH 



the patient. It will be seen that the disease resembles malignant 
pustule or carbuncle in several of its features. The etiology is uncertain. 

Schimmelbusch 1 found a bacillus (pure culture) upon the borders 
of the necrosis which may prove pathogenic of noma. 

Hillesen obtained a diplococcus which developed in pure culture, 
produced noma in an animal into which it was injected, and from 
the lesion a pure culture of it was obtained which in like manner was 
put through four animals. 2 

These cases are purely medical ; so that their full discussion is not 
warranted in these pages. The principle of treatment is to improve 
the general condition of the child, destroy the probable infection 
in the borders of the still vital tissue by cauterization, and promote 
sloughing of the necrosed tissue by the use of antiseptic applications. 

Fig. 691 




Noma. (J. Lewis Smith.) 



Dr. L. Fisher (New York) reported a case upon the inside of the 
cheek, cured by applications of ichthyol in lanolin four times a day 
over the entire area. 3 

The Eruptive Fevers. — Hyde and Montgomery describe the fol- 
lowing oral symptoms associated with various diseases having 
eruptive dermatitis as phenomena: 



1 Miller: Dental Cosmos, September, 1891, 

2 Dental Cosmos, 1908, p. 180. 



3 Ibid., 1902. 



STOMATITIS 727 

Scarlatina. — The mucous surfaces of the mouth and fauces are 
engorged tumid, reddened, and often covered with deep reddened 
puncta. The tongue is coated with a white fur over the filiform 
papillae. This is first partly lost, giving red puncta and a white 
background; when totally lost it gives " strawberry tongue." 

Variola. — The papules may appear over the entire alimentary 
canal. In the mouth they lose their epithelium, through heat, 
moisture, and friction. Reddened excoriated surfaces appear, over 
which the epidermis is reformed. Gangrenous complications are rare. 

Hemorrhagic Variola (Effusions of Blood into Mucous Surfaces). — 
The mucocutaneous orifices are crust-covered and exude an extreme 
fetor. Blood may escape from the mouth. 

Varicella. — The macular lesions may extend to the surfaces of the 
eyes, mouth, etc. 

Rubeola (Measles).— Even three days before skin eruptions. 
"Koplik's spots," bluish white or bright red with central bluish- 
white punctum on mucous membrane. In period of effioresence a 
catarrhal or eruptive inflammation. The mouth and throat have the 
eruptions. 

Syphilis. — Secondary eruptions, later forming mucous patches; 
characteristic crusts about nose and mouth (see page 732). 

Urticaria. — The eruption in well-marked cases may include the 
mucous membranes. 

Angioneurotic Edema. — The rosy red to livid edematous plaques 
may appear upon the lips and pharynx, producing at times dyspnea. 

Erythema Scarlatiniforme. — The mucous membranes in mouth 
and fauces may be reddened or be denuded of epithelium, but the 
characteristic "strawberry tongue" of scarlatina is wanting. 

Erythema Iris. — The papules may coalesce and be filled with 
blood or hematuria may result with severe involvement of mucous 
membranes of lips and mouth, ulceration rapidly ensuing. 

Erythema Multiforme. — Like the iris variety the macules may appear 
in the mouth. 

Dermatitis Herpetiformis. — When affected, mucous membrane of 
mouth sodden, macerated, pustules; bullae form and rupture, leaving 
raw erosions or sloughing patches of mucous membrane; extremely 
foul odor. 

Herpes Simplex. — Herpes Zoster. — See page 735. 

Erysipelas. — May extend to mouth, causing a dry, tumid, glazed 
appearance. 

Rhinoscleroma. — A rare disease; usually begins in nose; may extend 
to mouth, with ulcerative destruction, causing exfoliation of the teeth. 

Pemphigus Foliaceus. — The mucous membrane of the mouth and 
throat may be denuded. 



728 INFECTIONS OF AND FROM THE MOUTH 

Pemphigus Vegetans. — White patches followed by excoriation with 
foul odor may occur. 

Drugs Producing Stomatitis. — Many drugs taken internally may 
produce dermatitis or stomatitis as a temporary efflorescence, while 
with some, as mercury, the impression is more profound (see page 
646) ; with others it is simply expression of idiosyncrasy, with which 
the oral tissues may or many not take part. 

Iodin or bromin or their compounds; antipyrin and others of its 
class; arsenic, belladonna, aconite, carbolic, nitric, tannic, boric, arid 
benzoic acids; sodium benzoate and sodium borate. 

Chloral, digitalis, mercury, opium and its alkaloids, phosphorus, 
podophyllum, potassium chlorate, castor oil, cinchona and its alkaloid, 
quinine, salicylic acid and salicylates, strychnine, tar, turpentine, and 
others of less interest are mentioned. Silver nitrate internally given 
may produce argyria of the skin and mucous membranes. As 
instanced by argyria, the drug finds its way to the superficial tissue 
in which it may produce irritation. (Also see page 573.) 

SYPHILITIC AFFECTIONS OF THE MOUTH. 

The recognition of syphilitic lesions about the mouth is of vital 
importance to the dental operator, first, because by the recognition 
he may take steps to prevent the carriage of infection to innocent 
patients; and secondly, that he may avoid inoculation of himself 
by the poison. 

In the minds of many, syphilis is associated with the lower class of 
persons, who are confirmed debauches. While it is undoubtedly true 
that its prevalence is most marked in this class of persons, it appears, 
with horrible frequence, in persons who would be little suspected 
of having such infection. The operator is to be guided in his opinions 
and precautions in this matter, not by the social status of the patient, 
but by the nature of the morbid conditions existing. 

The cause of syphilis is the traponema pallidum discovered by 
Schaudin and Hoffman, and present in its lesions, transmitted from 
one person to another directly or through the medium of an inani- 
mate object which has been infected. 

The diagnosis may be made by microscopic examination. The 
sore is washed and the serum later exuded used to make a smear on 
a glass slide. Stein states that the edge of the sore should be scraped 
with a sharp instrument after washing, and the serum collected 
from that source, otherwise the treponema may not be obtained. 1 

1 Dental Cosmos, July, 1913, p. 744. 



SYPHILITIC AFFECTIONS OF THE MOUTH 729 

This is first dried in the air, then stained with Hastings' stain. After 
a minute distilled water is added until a metallic film is formed. 
After five minutes more they are washed in running water and 
dried. The treponema pallidum stains a faint blue. 1 They may 
also be seen living by aid of the "dark-field illuminator." It is said 
to have a slower motion and less undulation than other oral spiro- 
chetes. 

Syphilis is usually, divided into three stages, primary, secondary, 
and tertiary; to these may be added a fourth stage, viz., in patients 
who have been discharged as cured mild manifestations of disorders, 
particularly of the skin and mucous membranes, make their appear- 
ance from time to time, and disappear promptly upon the adminis- 
tration of iodids. The semen of syphilitics in the secondary period 
is infectious to apes and therefore accounts for heredo-syphilis. 

The first stage of syphilis — primary syphilis — consists in the for- 
mation of the primary sore or chancre, and the involvement of the 
nearest lymphatic glands. Secondary syphilis is attended by fever, 
eruptive inflammations of the skin, inflammation and superficial 
ulceration of mucous structures. In tertiary syphilis destructive 
inflammation of the skin, mucous membranes, and connective tissue 
occurs, together with the formation of specific tumors — gummata. 

Some differences of opinion exist among syphilographers as to the 
relative infective power of the secretions from the several lesions 
of syphilis. All are agreed, however, that the secretions from the 
secondary lesions observed in and about the mouth are highly 
infective. It is the part of prudence to regard all syphilitic lesions 
as infective. All these stages of syphilis may be seen in the human 
mouth. It is to be remembered that if the mucous membrane of 
the mouth be infected from a mucous patch (a secondary lesion), 
the acquired disease will appear, not as a mucous patch, but as a 
chancre. It is from mucous patches that infection is most to be 
feared. 

Primary Syphilis of the Mouth. — Causes. — The primary lesion 
of syphilis, chancre, when found in the mouth is a consequence of 
direct infection from a syphilitic. The infection occurs from contact 
of the mucous surface of the mouth with a syphilitic lesion upon 
another person. It has been transmitted by kissing, even with 
an innocent person as the intermediary; it may occur from using 
a glass or cup previously used by a syphilitic, by smoking cigars or 
cigarettes which have been made by syphilitic cigarmakers, who 
have applied the tongue to the tobacco in attaching the wrapper. 

1 McKee: Dental Cosmos. 1909, p. 1437. 



730 INFECTIONS OF AND FROM THE MOUTH 

Dental instruments may be the carriers. Any of the articles named, 
or the contact of any article which has been in contact with a 
syphilitic lesion, if brought in contact with an abraded mucous sur- 
face, may cause infection. 1 

The infection may be transferred from patient to operator if the 
fingers have any abraded surface, or if the surface is broken acci- 
dentally by an instrument. Dentists have been inoculated upon the 
hand. During and since the time of Hunter the use of teeth from 
syphilitic patients in plantation operations' has been a clearly 
recognized medium of communication. A fair percentage of all 
primary chancres appear within the dental field either upon the 
lips or within the mouth. 

Appearance and Diagnosis. — "The primary lesion of syphilis 
never makes its appearance before ten days after infection; the 
maximum period is about ninety days; the average is twenty-one 
days." 2 

It usually appears as a single, elevated, hard papule. In cases of 
oral infection, most frequently about the lips, the papule loses its 
epithelial coating after some days. The induration surrounding the 
papular mass increases until the papule, which is now raw and in a 
process of ulceration, appears surrounded by a ring of cartilaginous 
hardness. This induration is the one distinguishing feature of the 
chancre, which is not painful. In about a week after the appearance 
of the primary sore, swelling of the submaxillary lymphatic glands is 
observed. In case the chancre appears upon the tongue, the sub- 
hyoid lymphatic glands are swollen. 3 Unless pyogenic infection has 
occurred, the lymphatic involvement is not inflammatory, there 
being no pain present. In from three to four weeks the sore disap- 
pears, leaving no signs of its site in some cases; in others, some 
induration may persist. 

The diagnosis of this condition is the important consideration, so 
far as the dental practitioner is concerned, its treatment being the 
province of the medical practitioner. 

The elevation of the sore, its induration, and, if obtainable, the 
time of inoculation, are diagnostic data. The sore is single, as a 
rule, and there is hard, nodular painless swelling of the neighboring 
lymphatics. A single ulcer of ulcerative stomatitis may in some 
degree simulate the appearance of a very small chancre. It may 
exhibit slight induration, but its irregular form, situation, painful- 

1 Metchnikoff and Roux found that an ointment composed of 10 parts calomel 
and 20 parts lanolin, applied by inunction to an intentionally infected part, prevented 
the appearance of syphilitic infection if used within one hour after inoculation. Mer- 
curic chlorid was of no avail. Dental Cosmos, 1907, p. 1007. 

2 Gross: System of Surgery. 3 Park's Surgery. 



SYPHILITIC AFFECTIONS OF THE MOUTH 731 

ness, and the usual absence of lymphatic involvement, together 
with its prompt disappearance after sterilizing the mouth and cauter- 
izing the ulcer, will differentiate the two sores. If the chancre be 
upon the tip or sides of the tongue, where it is subjected to irrita- 
tion, it may become very large and bear a close resemblance to 
epithelioma of that organ. In epithelioma there are apt to be pains 
of a lancinating character, the induration follows ulceration, and 
the ulcer has hard edges and often a warty-like growth. 

It is a wise precaution to view all sores about the mouth as possibly 
infectious. All errors of diagnosis in this direction will be more than 
compensated for by the assurance of non-transference of infection. 

Secondary Syphilis of the Mouth. — The secondary manifestations 
of syphilis may be observed in and about the mouth, no matter what 
the location of the primary lesion may have been; they are the result 
of a general, not a local, infection. A skin eruption appears also. 

Fig. 692 




Chancre of the lip. 

Secondary infections of the mucous tissues appear in from four 
to twelve weeks after the appearance of the primary lesion. Sore 
throat, due to inflammation of the mucous membrane of the pharynx 
and parts about, is almost constant; together with syphilitic hoarse- 
ness, due to the extension of the affection to the mucous membrane 
of the larynx. 

The appearance of copper-colored areas upon some portion of the 
mucous membrane, on the tonsil, pharynx, soft palate, lips, or bucco- 
labial surface, precedes the loss of epithelium over these surfaces, 
which soon occurs, forming the most virulently contagious lesion 
of syphilis, the mucous patch. The patches become covered with 
a grayish-white, opalescent, pasty covering, resembling the ulcera- 
tions of non-specific stomatitis. So close is the resemblance that a 
differentiation can only be made at times by additional evidences of 



732 INFECTIONS OF AND FROM THE MOUTH 

secondary syphilis. Single patches may coalesce, forming large, 
irregular areas covered by a grayish-white pellicle. These patches 
are rarely painful. Ulcerations having ragged, irregular outlines 
may appear at the sites of the original patches or in other situations, 
and exhibit a tendency to spread. In healed cases the cicatrices 
present a whitish pellicle and contracted scar, indicative of old 
healed ulcers. In the skin little pits and linear scars are symptomatic. 

The diagnosis of the condition is determined by the history and 
by a discovery of other lesions of secondary syphilis, iritis, head- 
ache, neuralgia, paralysis of muscles of eye and face, chorea, brittle, 
cracking nails are often early symptoms; 1 also the lymphatic glands 
will be involved; skin eruptions, falling out of the hair (alopecia), 
and the areas of copper-colored eruption upon the mucous mem- 
brane of the pharynx and soft palate. 

Hugenschmidt 2 has observed among syphilitics, who presented no 
local lesions, the frequent nocturnal occurrence of indefinitely located 
dental pains, spreading to the palatal region. In case of doubt, 
search for the treponema, or the Wassermann or Noguchi's luetin 
reaction may be employed. (See works on Bacteriology.) 

Smoker's patches (leukoplakia) are considered by some as signs of 
syphilis but can only be considered in this connection if confirmed 
by the Wassermann test. 

Tertiary Syphilis of the Mouth. — The syphilides of the secondary 
stage arise in, and are confined to, the mucous and dermal structures ; 
those of the tertiary stage arise in the deep connective tissues, and 
are frequently associated with periosteum. 

Tertiary lesions, as seen by the dentist, are usually in the form of 
ulcers of, first, the soft or hard palate, and of the tongue or lips. In 
the earlier stages hard, nodular formations may be noted as ante- 
cedents to the ulcerations. Chronic periostitis of the palatal processes 
may occur, leading to the formation of localized thickenings. In 
other cases, in the soft palate, upon the tongue, or in the hard palate, 
localized swellings may occur, having a livid red appearance; the 
overlying mucous membrane breaks, establishing an ulcer, which 
may perforate the soft palate and destroy a portion of the palatal 
process, or form large ulcers on the tongue. The condition is one 
of gumma. These lesions appear in from two to five years after the 
secondary manifestations. 

Tertiary Lesions. — The sight and hearing may be affected, the 
throat diseased, causing loss of voice, necrosis of the bones and tissues 
of the nose causing deformity. The brain or spinal cord affected 

1 E. Whitney: Dental Cosmos, 1911, p. 524. 2 Dental Cosmos, 1892. 



TUBERCULOSIS OF THE MOUTH 733 

may cause paralysis, locomotor ataxia, or loss of reason. These are 
usually the result of failure to follow treatment to a conclusion. 

The tongue may have either a localized or widespread parchment 
like hyperplasia of the mucous membrane, and muscular tissue which 
may cause it to be become indented by the teeth, to lose its papillae, 
and become dry and red. Pedersen 1 calls attention to the fact that 
the indentations do not disappear when the tongue is stretched, 
while if due to ordinary debility they may do so. 

Although there is much doubt as to the degree of infectiveness of 
these tertiary lesions, precautions as to sterilization should be taken 
as with the primary and secondary lesions. A defined, ragged ulcer 
occupying the hard or soft palate, which has persisted for a long 
time, should always be viewed with suspicion, and a search be made 
for other evidences of syphilis. 

These ulcerations appearing upon the side of the tongue may 
closely simulate epithelioma of £hat organ. The confusion is increased 
if, in consequence of the presence of jagged teeth, a continuous 
irritation is excited. Moreover, leukoplakia of the cheeks, a diag- 
nostic sign of possibly incipient epithelioma, frequently accompanies 
tertiary syphilis. 

The existence of tertiary syphilis is of great clinical importance to 
the dentist in that a condition of lessened resistance of tissues is 
established, and disease processes which in the healthy person are 
comparatively circumscribed, in the syphilitic run a riotous course. 
A septic pericementitis by extension may involve a wide area of 
periosteum, leading to extensive maxillary necrosis. 

Treatment. — The treatment of syphilis has been largely by the 
administration of mercury and potassium iodid for a long period 
until the treponemata shall have been killed out. If not so con- 
tinued the tertiary lesions may reappear with serious results. The 
latest development in treatment is the use of Ehrlich's preparation 
of arsenic, dioxydiamedoarsenobenzol, "606," or "salvarsan," for 
which positive claims as a prompt cure are made. There is promise 
of a cheap and valuable chemical remedy from the Rockefeller 
Institute. 

TUBERCULOSIS OF THE MOUTH. 

The bacillus of tuberculosis, under favorable conditions, develops 
in the tissues of the mouth, producing its characteristic lesions. 
Finding a suitable soil, such as is furnished by the heredity which 
predisposes to phthisis pulmonalis, the bacillus may find entrance 

1 Dental Cosmos, 1908, p. 332. 



734 INFECTIONS OF AND FROM THE MOUTH 

to the deeper tissues from the mucous membrane of the mouth and 
excite tuberculosis in the deep structures, the bone, etc. A number 
of perforations of the hard palate have occurred. According to Curtis 
these are usually fatal. What part is played by local oral and dental 
lesions in tuberculosis of distant parts, by establishing pathways 
for the entrance of the bacilli into the circulation, is at present 
conjectural, but that such infections occur is very probable. Lupus, 
a skin tuberculosis, may extend to the mouth producing nodules. 

ACTINOMYCOSIS. 

The condition produced by the development of the ray-fungus, the 
actinomycosis, in the lower jaw and cervical regions of cattle and 
swine — lump-jaw — is not unknown in human beings. It may be 
derived by chewing straw or grass in which the ray-fungus has 
produced "rust." 

Miller 1 gives 203 cases reported in German medical literature 
between 1886 and 1891. In at least 120 of these cases the point of 
entrance of the fungus was found to be in the region of the mouth or 
throat. Actinomycosis threads have been repeatedly found in the 
saliva and in carious teeth, and notably in the tonsils. Whether the 
path of entrance to deeper structures is ever through carious teeth 
is undertermined, but certainly lesions or wounds about the mouth 
furnsh an entrance. Padgett reports a case of alveolar ulceration 
following extraction, which proceeded to abscess upon the face. 
Bacteriological examination showed the ray-fungus. 

The disease has yielded to the action of sulphate of copper, J 
grain, plus iodid of potassium, 10 grains, internally four times a day, 
together with local irrigation of 0.1 per cent, solution of copper 
sulphate. 2 

GONORRHEA. 

Cases of oral infection by the gonococcus of Neisser have been 
reported. The oral mucous membrane and the gums may undergo 
intense suppuration with its accompaniments. Fever and its accom- 
paniments may be present. The eyes are very subject to secondary 
infection in an individual suffering from gonorrheal urethritis. The 
hands are a medium of transference. Babes may be directly infected 
by the mother during birth, and blindness often results. The law 
now requires the instillation of a mild solution of silver nitrate or 
other antiseptic as advocated by Crede. The diagnosis can be made 

1 Dental Cosmos, 1891. 2 Brophy: Dental Cosmos, 1908, p. 78. 



HERPES ZOSTER 735 

by microscopic examination of the bacteria Brown 1 cites a case in 
which the gonococci were found. Stein claims that endeavor to infect 
the nose with gonococci failed and questions oral infection by them. 
(See page 610.) Lederer in a case of oral infection in a patient with 
urethral gonorrhea found it by microscopic examination to be a case 
of Vincent's angina, which see. Calomel internally and silver nitrate 
applications, 1 to 250 increased gradually to 1 to 50 are recommended. 
(Brown.) 

HERPES LABIALIS (FACIALIS) (HERPES SIMPLEX). 

This consists of a vesicular eruption upon the lip, tongue, mouth, 
cheeks, or allse of the nose. The vesicles are filled with a clear fluid 
which soon discharges. An excoriation is left often covered by a 
light crust, which is never followed by a scar. The condition ma;y 
cause little pain or considerable burning and itching. It may accom- 
pany colds, fevers, exposure to heat, draughts, and gastric disorders. 
It follows either a direct irritation of the nerves, as after the use of 
rubber dam or other dental operations in susceptible persons, or may 
be of reflex origin; in either case localized peripheral neuritis being 
the initial lesion. 2 There is some reason to believe that infection 
plays a part in its production. As a preventive it is well to lubricate 
the lips with glycerin and rose water or with cold cream or carbolated 
vaselin 1| per cent, strength (commercial) when much stretching or 
other irritation is necessary. 

ECZEMA. 

A pustular form of eczema or a seborrheic form may occur about 
the border of the lips. The cause is held to be a cutaneous weakness 
due to various constitutional factors with local excitation by irritants 
of various kinds, no bacterial etiology is as yet assigned. 

HERPES ZOSTER. 

This is a probably infectious disease, almost invariably mono- 
lateral, associated with a neuritis usually of a spinal ganglion or with 
a peripheral neuritis, which produces, first, a hyperesthesia of the 
integument, macules, and later vesicular eruptions not usually 
beginning on a mucous surface. They appear in groups and may 
coalesce, forming patches. Desiccation forms a crust; pus may 
form. 

1 Oral Diseases and Malformations. 

2 Hyde and Montgomery: Diseases, of the Skin. 



736 INFECTIONS OF AND FROM THE MOUTH 

The interest to dentists lies in the fact that in zoster of the head 
exfoliation of the teeth is said to be associated in rare cases. 1 

Some have considered it due to oral sepsis. Lain 2 found apical 
abscesses in 95 per cent, of his cases. 

LEUKOPLAKIA BUCCALIS. 3 

Upon the inner surface of the cheeks or lips, and upon portions of 
the gum and the dorsum and edges of the tongue, may appear sharply 
outlined, dull, whitish, slate-colored or silver-whitish points, disks, 
streaks, bands, ribbons, or patches of irregular shape, either flattened 
or slightly elevated, above the general level of the mucous surface. 
They may crack or fissure, and inflammation of the derma and pain 
result. Ordinarily they are simply rough and without much dis- 
comfort. It occurs almost exclusively in males. They differ from 
the mucous patches of syphilis in that the latter are soft and tend to 
ulcerate, and, while they may accompany syphilis, may occur in its 
absence or of any history of it. 

They simulate the keratosis of lichen planus, which should, however 
also appear as papules upon other parts of the body. 

Apart from syphilis, it is due to irritation such as that from 
tobacco or rough teeth, and with syphilis, tobacco, and rough teeth 
may be additional excitants. 

R. H. Ivy reports three cases with tendency to epitheliomatous 
degeneration, all without history of syphilis, and in two of which 
the Wassermann reaction was negative. 4 

The use of alcohol and spices are also a cause. 

The pellicle is closely adherent, and consists of an hypertrophied 
and hyperkeratinized epithelium, with more or less inflammatory 
infiltration of the derma and with partial obliteration of the papillae. 

The chief danger in the disease is the tendency to epithelioma, 
some authors estimating 30 per cent., especially in the cases in which 
exfoliation and ulceration occur. Some eighteen years ago a male 
patient presented with a leukoplakia in which there was a constant" 
desquamation as though very hot liquids had been used. Medical 
treatment was given, tobacco and liquor were largely avoided, but 
after about twelve years, epithelioma involving a jaw operation 
occurred. This patient was apparently cured, but the epithelioma 
recurred and the patient recently died a lingering death. 

1 Hyde and Montgomery: Diseases of the Skin. 

2 Quoted by Nodine, Dental Cosmos, November, 1917, p. 1095. 

3 Hyde and Montgomery: Diseases of the Skin. 

4 New York Medical Journal, October, 1912, p. 1187. 



PHOSPHOR NECROSIS 737 

The use of soothing mouth washes, together with a hygienic regimen 
and the avoidance of irritants like tobacco, alcohol, spiced, hot, or 
iced foods. The correction of habit and institution of local and general 
hygiene is the usual treatment to avoid epithelioma. The use of 
caustics has been objected to as likely to cause epithelioma in these 
cases. Some consider that it is very infrequently a cause of epithe- 
lioma in itself. The diagnosis lies clearly within the province of the 
dentist who may note it before the patient. The treatment is 
usually conducted by the physician, and is often unsatisfactory as 
to permanent cure. Cases with syphilitic history, of course, require 
antisyphilitic treatment. 

Leukoplakia has been also called buccal psoriasis, but psoriasis 
does not affect mucous surfaces, hence it is a misnomer. 

LICHEN PLANUS. 

This condition, which may simulate leukoplakia, 1 is characterized 
by an eruption consisting of glistening flat-topped polygonal papules 
with tendency to form irregularly arranged groups. On the mucous 
surface they appear as whitish macules, striae, or flat papules on both 
sides of the tongue at the points in contact with the molar teeth. 

They are the result of an arterial or venous hyperemia of the 
papillae of the corium, a secondary thickening of the lower part of 
the rete, and a tertiary flattening of the papule by pressure. 

A proliferation of cells in the granular layer and a deposit of 
keratohyalin in whitish spots occur. This causes a similarity to 
leukoplakia. It usually occurs in the nervously exhausted, though 
many patients may have a fair degree of body nutrition while yet 
nervously exhausted. 

Lain found local oral infection in 85 per cent, of his cases (see p. 736). 

PHOSPHOR NECROSIS. 

This disease is a more or less extensive necrosis of the maxillae due 
to the entrance of phosphorus or its fumes into contact with the 
periosteum or pericementum of a tooth. 

It was formerly frequent in match factories, when white phosphorus 
was used, though now less when the red is employed, but has occurred 
through the chewing of match heads, and a case has been reported 
in which a half grain taken in three days caused it. 2 

As it does not ordinarily occur in the mouths of those having 

1 New York Medical Journal, April 13, 1912. 

2 Arnone: Dental Cosmos, 1910, p. 425. 

47 



738 INFECTIONS OF AND FROM THE MOUTH 

sound teeth, it is generally regarded as of local origin, the phosphorus 
gaining entrance either through the pulp canal of a tooth, or, possibly, 
through some point of injury external to the tooth. 

Abscesses containing offensive pus cause great swelling and exces- 
sive salivation, and may cause several fistulas, while the swallowing 
of the discharge causes general toxic disturbance, and infection such 
as pneumonia or cerebrospinal meningitis may have rapid effect. 

The periosteum remains unaffected as to its vitality, while the 
bone proper undergoes osteoporous necrosis, becoming like rotten 
sponge. As the sequestrum is separated, there is a tendency to 
formation of new bone by the periosteum. The necrosis of bone may 
be very extensive, involving in the lower jaw the entire horizontal 
portion, while the ramus may remain unaffected. In the lower jaw, 
after exfoliation, the bone may be almost entirely restored to an 
amount nearing fair comparison with the ordinary edentulous 
mouth, while in the upper jaw no repair occurs. This new bone may 
undergo atrophy if not put to work by artificial teeth. 1 As a pro- 
phylactic sodium bicarbonate solutions are recommended by Arnone. 2 

SCORBUTUS. 

Scurvy in the adult is a disease due to diet and in former days was 
frequent in armies and among sailors on long voyages. 

The use of a restricted diet lacking fresh vegetables and fruits was 
a chief cause. It is supposed to be due to lack of potassium salts. 
Rhinehart 3 classifies the following symptomatology: Slow onset, 
swelling about eyes, face pale, bloated, mental and physical debility, 
gums spongy, swollen or fungoid, teeth loose or may drop out, occa- 
sional necrosis of jaw, breath offensive, tongue swollen, but usually 
clean and pale, appetite lost but digestion usually good, skin dry and 
muddy, after ten days capillary hemorrhages usually about hair 
follicles of legs. Subnormal temperature or fever, heart possibly 
feeble or palpitating. Aside from oral antisepsis the treatment is a 
general reversal of diet, giving vegetables rich in potassium salts and 
the organic acids of fruits (see page 739). 

PURPURA HEMORRHAGICA. 

This is the appearance of small purplish spots beneath the skin 
and mucous membrane, and is dependent upon infection and toxic 
conditions. 

1 For consideration of treatment the reader is referred to Garretson's System of 
Oral Surgery, sixth edition, and other writings upon the subject. 

* Dental Cosmos, 1909, 3 Ibid., 1914, p. 1217, 



ANGINA 739 

Brown/ following Schamberg, presents the following clear differ- 
ential symptoms: 

Scorbutus. Purpura Hemorrhagica. 

1. Occurs in those subjects due to lack 1. No such etiological relationship. 

of vegetable food and to bad hy- 
giene. 

2. Definite antecedent symptoms, weak- 2. Antecedent signs slight or absent. 

ness, impaired circulation, etc. 

3. Onset slow. 3. Onset sudden. 

4. Gums spongy, swollen, and bleeding; 4. Gums often bleeding, but not swollen. 

teeth loose. 

5. Severe muscular pain. 5. Less marked. 

6. Brawny infiltration of lower extremi- , 6. Not present. 

ties. 

7. Hemorrhages from mucous mem- 7. Hemorrhages from mucous mem- 

branes, not profuse, as a rule. branes so severe as to sometimes 

prove fatal. 



LEPROSY. 

During the progress of leprosy, an infective disease, characteristic 
nodules and ulcers appear about the oral structures. As many parts 
of the head are affected in like manner, these are but symptoms of 
the progress of the effects of the Bacillus lepra. 2 

ANGINA. 

Angina is usually defined as a sense of choking or suffocation, 
a symptom which accompanies inflammatory affections of the 
pharynx as well as the paroxysmal neuralgic affection of the heart 
known as angina pectoris. 

Angina Simplex. — This is inflammation of the pharynx, with, of 
course, more or less swelling and infiltration of exudate. Swallowing 
may be difficult. Local depletion and sedative washes, with general 
derivation, are indicated. If chronic, stimulant washes are useful 
combined with general tonic treatment. 

Ludwig's Angina. — In 1836 Ludwig described a disease which is 
considered to be an infectious cellulitis in the submaxillary region, 
which may extend deeply into the tissues of the neck. The infection 
is thought to be due to the Streptococcus pyogenes or bacillus of 
malignant edema, though the Staphylococci and Pneumococcus are 
found, and probably enter the cellular tissue of the submaxillary 
region and neck through the oral or pharyngeal mucous membrane 
or a wound. An apical abscess, also, the repeated impaction of food 
into the pericoronal region, especially about a third molar, and its 

1 Dental Cosmos, 1911, p. 296. 

2 For an exhaustive article see Oliver, Dental Cosmos, 1908, 



740 



INFECTIONS OF AND FROM THE MOUTH 



fermentation have caused a deep infection resulting in this disease. 
The patient has lassitude, chilliness, and fever. 

A hard swelling appears beneath the mandible after several days, 
and extends toward the neck and under the tongue. There is mus- 
cular rigidity and the head is inclined in one direction. The skin is 
not much reddened. 

Later edema is marked and may extend upward toward the 
parotid gland or the glottis. Breathing and swallowing are rendered 
difficult by oral and pharyngeal swellings. There are the usual oral 
symptoms of inflammation. Upon incision the connective tissues 
are found to be sloughing, grayish black in color, and may ooze pus. 

The board-like hardness of the floor of the mouth and the marked 
dyspnea are constant features. 

The spread of the infection being by continuity of cellular spaces, 
the glands are much enlarged. 

A large abscess may form and discharge. Pneumonia, septicemia, 
and pyemia are complications to be feared as the result of spreading 
infection. Incisions for drainage and antisepsis are usually con- 
joined with systemic treatment, but as the case is often of dental 
origin the cause should be removed. 

Fig. 693 



Spirochetes of Vincent's angina. (M. T. Barrett.) 



Vincent's Angina. — This is an edematous tonsillitis, which may 
affect also the mucous membrane of the mouth and pharynx, fol- 
lowed by the formation of a pseudomembrane as in diphtheria, later 
ulceration and hemorrhage may appear. There are the usual accom- 
paniments of inflammation in this locality, together with fever and 
sometimes rigors. It usually lasts about two weeks. It also occurs 
about the gums without necessarily affecting the pharynx, and here 
may last much longer. Here it produces a dirty ulceration of the 
gum margins producing a foul odor (see page 608). 



INFECTIONS FROM THE MOUTH 741 

The differential diagnosis from diphtheria and syphilis is made by 
microscopic examination. The Bacillus fusiformis, spindle-shaped, 
pointed at extremities, and 6 to 10/x in length, is usually associated 
with a long thin spirillum. (See Figs. 580 and 693.) 

They take several stains, but not the Gram. In diphtheria, 
Loeffler's bacilli, and in syphilis the treponema pallidum would be 
found. Tuberculosis, gonorrhea, stomatitis, and pyorrhea must 
also be differentiated. (Lederer.) 

In the treatment mercuric chlorid 1 to 10,000 in 4 per cent, boric 
acid solution, and especially salvarsan, 10 per cent, in sesame oil, 
suspended by the aid of Iodipin (Merck) is recommended for injec- 
tion into the pockets or applied to the gum, are highly recommended 
by Lederer. The writer has cured a number of cases of this type 
by the use of mercuric chlorid, 1 grain in each four ounces of H 2 2 . 
A microscopic examination was not made. 1 Vaughan recommends 
silver nitrate, 4 to 8 per cent., Lugol's solution, chromic acid, 10 per 
cent., zinc chlorid, 2 per cent., and Argyrol full strength, also a light 
diet and cathartics. (Other treatments on page 615) . 2 

INFECTIONS FROM THE MOUTH. 

General Septic Diseases of Dental Origin. — The effect of the exist- 
ence of dental diseases upon the body at large, particularly as regards 
secondary infection, is a matter increasing in importance as the possi- 
bilities of their connection are made out. At present the organisms 
of greatest demonstrable pathological interest are the streptococci 
and pyogenic cocci. The almost constant presence of these organisms 
in the mouth, carried thence into the pharynx, posterior nares, larynx, 
lungs, and stomach, furnishes the reason for the pyogenic and phleg- 
monous inflammations which occur in these organs. The diplococcus 
of pneumonia, a frequent organism, but waits a favorable opportunity 
to establish high inflammations and fibrinous exudations in the lungs, 
and possibly in other structures. The oral pneumococcus is now 
rather regarded as not the one producing pneumonia. 

The most important clinical associations of dental with general 
infections are diseases of the pericementum, but the pulps of teeth 
are claimed by Price 3 to take up and transmit the products of the 
action of septic organisms. It must be remembered that the veins 
may transmit the poison, and, in addition, may perhaps convey 

1 For an exhaustive article see Vaughan, Dental Cosmos, June, 1912. 

2 For beautiful illustrations of many of these oral conditions, See Brown's Oral 
Diseases and Malformations. 

3 Lecture before the Pennsylvania State Dental Society, 1917. 



742 INFECTIONS OF AND FROM THE MOUTH 

organisms from a diseased but still vital pulp to distant parts. When, 
however, the pulp is dead and the pericementum is invaded, there is 
no doubt of general infection from this local source. More or less 
septic intoxication is a common attendant upon severe septic apical 
pericementitis, and septicemia accompanied by inflammation of the 
neighboring lymphatic glands is of sufficient frequency to emphasize 
the need of the vigorous antiseptic treatment recommended in all of 
these cases. 

Pyemia is far more uncommon. 1 Pyogenic organisms, gaining 
access to the blood current from the local source of infection, establish 
suppuration in distant parts; in other parts of the bone, or in other 
bones (osteomyelitis), in the lungs, meninges, and substance of the 
brain. One case 2 has been reported where abscess of a toe, ear, and 
forearm ceased, and recovery took place after treatment and filling 
of septic root canals. Several cases are tabulated by the same author 
in which extensive necrosis and death resulted from pyemic infec- 
tion from septic pericementitis. Some of these cases recorded were 
associated with acute, some with chronic, septic pericementitis. 

In addition to the usual pyogenic cocci, Miller has isolated several 
forms of cocci, bacilli, and spirilla, forming products which, if injected 
into the circulation of animals, cause death from septicemia in from 
hours to days. As many of these forms may be brought into rela- 
tion with deep parts by the anatomical conditions created by pulp 
death, the possibilities of many types of infection via pulpless teeth 
are evident. (See pages 532 and 557.) 

The possibilities of local as well as general infections through the 
conditions established in the several forms of pyorrhea alveolaris 
should not be forgotten. (See page 696.) 

The pockets formed by the soft tissues overhanging lower third 
molars whose eruption is impeded invite the passage of septic organ- 
isms to deep parts. Local pyogenic infections are common in these 
cases, and may extend into the pharynx and the submaxillary tissues, 
as in Ludwig's angina. 

The question is one of systemic infection from a dental focus of 
infection; in addition the mouth being a port of entry for many 
bacteria, the diseases they produce may in a general way be considered 
as having origin in the mouth, but in a specific way only such 
diseases as already exist in the mouth and possibly producing 
systemic disease are here considered. 

Rheumatism. — This is an inflammatory disease now generally 
regarded as due to bacteria carried by the blood to the diseased tissue 

» Miller: Dental Cosmos, 1891. * Tbid. 



INFECTIONS FROM THE MOUTH 743 

from some primary source (focus) of infection, e. g., the urethra 
(gonococci) the tonsils, the mouth (pyorrhea pockets and apical 
granulomata, etc.), or possibly from other infectious conditions. 

The forms vary from muscular inflammation of which wry-neck 
is one form to inflammation of the synovial membranes of joints and 
later of the cartilages which may, if infected by pyogenic bacteria, 
even be purulent. Arthritis deformans is a chronic inflammation of 
similar origin resulting in destruction and construction changes in 
the bones, producing flexed finger, spinal curves, etc. Viewing the 
disease in its entirety it would seem that the simple forms are due to 
Streptococcus viridans, organisms of low virulence producing non- 
suppurative inflammations and often originating from focal infection 
in the mouth. The more suppurative forms are probably due to 
pyogenic organisms having origin in pus foci in the mouth, tonsils or 
other locations. There is necessarily pain and loss of function and 
often the other symptoms of acute inflammation and when established 
may continue in spite of removal of a primary focus, i. e., they act 
as foci in themselves. However, many cases subside upon the removal 
of the primary focus, and an autogenous vaccine may be an aid to 
recovery. 

Endocarditis. — An infective inflammation nearly always of the 
valves of the heart, usually the mitral and aortic. It follows rheu- 
matism in any form, also often pneumonia and may follow any of the 
principal infective diseases. Staphylococci, gonococci and strepto- 
cocci even the Streptococcus viridans so commonly found in dental 
granuloma, tonsils, etc., may act as the infecting organism. The 
bacteria, either in the blood stream, passing through the heart valves 
or more probably entering their capillary circulation, produce epi- 
thelial vegetations which may later be carried off as emboli with 
dangers of embolism. If the emboli are infective metastatic infec- 
tions are possible (as infective infarctions, etc.). Infectious infarc- 
tions often appear in the end arteries of the kidney and may lead to 
abscess. They are usually the result of malignant endocarditis 
(pyogenic bacteria). 

When chronic, valvular incompetency with regurgitation is pro- 
duced by prevention of apposition of the edges of the valves by the 
excrescences. Hypertrophy of the heart is a result of the effort at 
compensation for mitral regurgitation and its consequent effect upon 
blood impulse. McFarland states that a safe balance is found in 
combined hypertrophy of the left ventricle, dilatation of the left 
auricle, passive congestion of the lungs and hypertrophy of the right 
ventricle which may later be dangerously upset by insufficency in the 
tricuspid valve (right ventricle) . 



744 INFECTIONS OF AND FROM THE MOUTH 

Fibroid induration, degenerations and calcifications are the com- 
mon sequela?. Appropriate murmurs and pulse signs are noted with 
the various conditions established. (See McFarland's and other 
Text-books on Pathology.) 

Neuritis. — This is an inflammation of nerve tissue either due to 
trauma or to focal infection. The inflammation may be acute with 
its phenomena (occasionally suppuration) or chronic with degenera- 
tive changes in the nerve tissue. If the tissue controls important 
parts secondary effects may arise. 

As related to dentistry it is one of the consequences of oral infections, 
its etiology and pathology being similar to that of rheumatism, i. e., 
infection derived from the teeth or gum pockets is absorbed and causes 
nerve inflammation rather than joint affection. 

Lymphadenitis. — This is an inflammation of the lymph nodes, 
usually occurring in infections in the nearest nodes through which the 
infected lymph drains. Swelling of the smaller nodes should lead to 
examination of the part from which they drain. 

Lymphangitis is inflammation of the lymphatic vessels due prob- 
ably to infective or at least toxic product from a focus. Thus in a 
felon, a bright red streak may run from the hand to the axilla, follow- 
ing the line of the vessel. Occasionally chronic lymphatic engorge- 
ment leads to dilatation with possible proliferation of the surrounding 
connective tissue. (Lymphangiectasis.) 

Furunculosis. — The presence of multiple abscesses (boils, car- 
buncles, etc.) in the skin may be due to direct infection by bacteria, 
always more or less present upon the skin probably with plugging of a 
fat duct or entrance into a hair follicle, but a lowered resistance to 
infection and a possible skin infection by carriage through the blood 
of bacteria from some focal infection as about the teeth, tonsils, etc., 
is quite possible. Schamberg 1 coincides with this view. Grieves lists 
this latter as a cause (see page 557). 

Nephritis. — Viewed as an infective condition nephritis or inflam- 
mation of the kidney is probably due to the toxins derived from 
general infections (e. g., yellow fever) or the bacteria from some 
focal infection (possibly about teeth). 

The damage is to the excretory portions, glomerules and tubes, 
the function of which is to excrete the irritating substances coming to 
them. If these subside as in yellow fever the symptoms (albuminuria) 
disappear and probably little injury is done. If continued a long 
time as in uricacidosis or other leukomain production, alcoholism, 
etc., the parenchyma degenerates (fatty) and the connective tissue 

1 Private Communication. 



INFECTIONS FROM THE MOUTH 745 

increases. McFarland describes it as "characterized by increased 
quantity of urine of low specific gravity, little or no albumin and very 
few tube casts of which the hyalin, pale granular and waxy varieties 
only are found." Stengel remarks the presence of streptococci in 
cases of obscure infectious origin which is confirmatory of recent 
observations regarding the focal infections about teeth as a cause. 
In fact, Hartzell and Henrici have experimentally produced nephritis 
in animals by injecting oral streptococci into their blood. (See p. 560.) 

Infectious infarction of the kidney is usually produced by emboli 
from suppurative endocarditis and leads to abscess in the kidney 
(McFarland). In kidney lesions due to oral infections, Hartzell 1 
notes albuminuria and casts in quantity, lessening as the local foci 
of pus formation are removed. 

Alimentary Canal Infections. — From the teeth down there is 
no difficulty in understanding tonsillitis, gastritis, gastro-enteritis, 
enteritis, cholecystitis, colitis, appendicitis and proctitis as septic 
inflammations due to oral bacteria entering the alimentary canal. 
Of course they need not be due to teeth in all cases, but pyorrhea, 
chronic abscesses and nasal and tonsillar suppurations are easily a 
possible cause. It is curious how convinced people may be as to the 
effects of disease of the stomach upon teeth, e. g., as a cause of caries 
or pyorrhea, while skeptical of oral disease as a cause of the stomach 
disease, etc.; no matter how carefully explained. This is due to long 
continued custom of thought. 

McFarland states that bacteria, unusual to the intestines having 
marked infectious powers, such as streptococcus, typhoid bacillus, 
B. dysenteric, cholera spirillum, tubercle bacillus, and also ameba 
coli and ameba hystolitica of dysentery, may occasion extensive 
and characteristic lesions. The enteritis may be catarrhal, follicular, 
pseudomembranous, or ulcerative. Appendicitis has the intestine 
as its source of infection and mechanical irritations which, as shown, 
may originally be in the mouth. Bilious attacks have been due to 
teeth. 

The reverse order of disease is always possible in that alimentary 
canal disturbances affect physiological digestion and absorption as 
well as produce abnormal fermentative products which are absorbed. 
Thus cell nutrition is disturbed by lack of proper food supply and by 
toxic substances in the blood stream which also may introduce the 
element of retained leukomains due to improper elimination at the 
kidney, skin, liver, lungs, etc. The whole range of malnutritional 
disorders is involved which necessarily affects systemic resistance to 

1 Journal of Allied Societies, June, 1914. 



746 INFECTIONS OF AND FROM THE MOUTH 

bacteria and local resistance as well. This is a vicious circle. (See 
also Headache.) Babcock 1 stated that in all cases of cancer of the 
stomach his patients had pyorrhea. This could be a direct chronic 
cause of irritation from the mouth or it might be argued to begin 
with the cancer as a vicious circle. 

Iritis. — Inflammation of the iris has occasionally been connected 
with oral infection as shown by its cure as the oral infection is removed 
(see page 557.) 

Headaches. — These are often due to alimentary disturbances, 
often the result of infectious fermentations. The alimentary canal 
is a port of entry to the blood. 

Crof ton 2 states that : 

1. Microbes constantly pass through the wall of the alimentary 
canal into the radicals of the portal veins and lymphatics being con- 
veyed by leukocytes. 

2. That if normal resistance of the mucous membrane is lowered, 
microbes ordinarily harmless may become pathogenic and then 
produce a general infection. 

3. That swallowed pathogenic bacteria may lower the resistance 
of the mucous membrane. 

4. That the stomach may be invaded from the intestine. 

5. That B. coli communis, streptococci and anaerobic bacteria are 
so constantly present as often to be considered normal. 

Since headache is known to have such an origin in many cases, it 
is reasonable to suppose that persistently recurrent headaches may be 
due to oral foci of infection and have indeed disappeared on removal 
of such foci. In one case after a single treatment of an abscess on a 
lower cuspid, headache of constant character disappeared, (see pages 
123 and 557). 

Nervous Disorders. — Cases of melancholia, or occasional delusions, 
as of approaching insanity, may be caused by focal infection. In one 
peculiar case a patient was unable to swallow, and the extraction of 
two abscessed teeth and one markedly pyorrhetic tooth, together with 
the clearing up of a reasonable general pyorrhea, rapidly cured the 
dysphagia. Nervous breakdown is an occasional symptom. 

1 Private Communication. 

2 Therapeutic Immunization, p. 71. 



CHAPTER XXV. 
PROPHYLAXIS. 

By prophylaxis is meant the prevention of disease and as a broad 
conception includes any measures whatsoever the application of which 
will prevent the occurrence or recurrence of disease in general. As 
applied to a particular disease the measures employed are spoken of 
as the prophylaxis of that disease, e. g , prophylaxis of dental caries, 
tuberculosis, etc. By common consent the periodic application of 
such treatment as is necessary to prevent the occurrence of disease 
is called prophylactic treatment. 

In dentistry prophylaxis involves first the removal of the. cause or 
causing factors leading to: 

1. Dental caries which leads eventually to pulp diseases and their 
consequences. 

2. Gingivitis and pyorrhea alveolaris (periodontoclasia) and such 
systemic conditions as are consequent upon them. 

3. (a) General malocclusion of the teeth, (b) malocclusion due to 
loss of necessary occluding teeth or individual malocclusions both 
involving overwork of the pericementum leading to its degeneration. 

4. The effects of diet or water taken by the mother or the child, 
or disease of either having influence upon either the first or second 
dentition. 

5. The effects of systemic or general oral acidity or wear. 

6. A sixth classification involves the discovery and removal of all 
local foci of infection which may be consequent upon dental caries 
or pulp disease or pyorrhea alveolaris as a means of prevention of 
systemic infection expressing itself, as a rule, in arthritis, muscular 
rheumatism, endocarditis, abscesses in distant localities, etc. (see 
pages 557 and 743. 

There can be at the present time no doubt that the only correct 
view of dental prophylaxis is to regard the mouth in its entirety as a 
possible source of infection which may overwhelm the entire system. 
This includes two views: 

1. That the infection actually exists in one or more of the follow- 
ing conditions: 

(a) Cavities of decay or other foci of dental caries acting as centers 
of infection for the mouth and alimentary canal. 

(747) 



748 PROPHYLAXIS 

(b) Gingival infections, as in gingivitis or pyorrhea alveolaris, 
also acting as foci of infection for month and alimentary canal and 
by way of the blood. 

(c) Apical abscesses, acute or chronic (including granulomas), or 
even infected living or putrescent pulps, which do not show, radio- 
graphically, abscesses in connection with them, all of which may act 
by way of the blood stream or when connected with the mouth act 
by that channel. 

(d) Sepsis about bridges, plates, etc., infecting the alimentary canal, 
2. That the mouth is an infected locality and that at any time 

caries or gingivitis may begin unless prophylactic treatment is insti- 
tuted and if neglected lead to the foregoing local conditions and so to 
systemic infections. 

As with the exceptions of Class 4 and general orthodontic mal- 
occlusion in Class 3, and pulp diseases due to accidents such as blows, 
etc., and erosion and abrasion all dental diseases are probably due 
to microbic plaques upon the teeth (see page 244) ; it follows that the 
systematic removal of such plaques and their associate factors consti- 
tutes the rational prophylactic treatment for prophylaxis of the said 
diseases. Clinical experience has amply demonstrated that a thor- 
ough prophylactic treatment at periods varying from one to three 
months will prevent the inception of caries and gingivitis if the 
patient gives intelligent assistance. In case of very active pyorrhea, 
when the conformation of necks of teeth are such as to render per- 
sonal attention practically impossible, more frequent attention by the 
dentist has at times been necessary and appreciated by the patient. 

As patients usually present with some form of dental disease, the 
first step after treating the acute condition is to place the mouth 
in as cleanly a state as possible and to obliterate any gum disease, 
while at the same time cavities of decay are to be prepared and filled 
as rapidly as conveniently possible with exactly adapted, perfectly 
contoured, highly polished, insoluble (insofar as utilizable) fillings, 
the margins of which are extended into areas subjected to friction by 
ordinary forces, such as food excursions, brushing, etc. Departures 
from this principle are to be made for well-judged reasons only and 
when made prophylaxis must be more vigorous. There can be no 
question that as to the choice between small unextended approximal 
fillings plus prophylaxis and waiting for cavities to become larger so 
that contoured fillings may be inserted the preference lies with the 
former, as in the latter method lies the danger of pulp approach and 
death in various ways thus inviting the condition so frequently seen 
of the presence of several treated or untreated devitalized teeth in a 
mouth with its dangers from systemic disease (see page 557) . There 



PROPHYLAXIS 749 

is, of course, the middle ground of extension of all cavities, however 
small, to which, however, there are many objections, though argu- 
ments pro and con are valid. 

In all operations the conditions of recurrence must be considered 
and if possible avoided (see page 357). 

Granting the necessity for attention to actual conditions in order 
that prophylaxis may be effectual a first step is the diagnosis of the 
extent to which the patient has departed from oral cleanliness and 
the demonstration of the same to the patient. The disease existing 
may be demonstrated first, then the presence of the causative factors 
in the microbic plaque, food collection and calculus. 

The microbic plaques are readily shown by means of iodin, either in 
the form of the tincture or a solution of the same in alcohol or water, 
or pure or diluted iodoglycerol, or in a special disclosing iodin solu- 
tion. 1 The introduction of this means of disclosure is attributed 
to the late Dr. Francis 2 of New York, who about 1884 remarked that 
"it does not so much remove the soft collections on the teeth as dis- 
closes their location." The iodin imparts its brownish color to both 
clean and plaqued surfaces and can be douched off the clean portion 
by means of water leaving the plaques stained (Fig. 261). The figure 
while of caries, so closely illustrates that it may serve instead of a 
special illustration. At this demonstration the value of brush and 
floss motions can be shown to the patient and is very convincing. 
That these collections have been denied to be plaques is known to the 
writer and that they are often found where no caries exists involves 
a consideration of their bacterial content (whether caries fungi or 
not). The fact that they are found as causes of gingivitis, etc., in 
which caries is not present and that also their removal cures the dis- 
ease is again evidence of a varied bacterial content. In either case 
the question of the carbohydrate food factor as in caries or the 
albumin factor (gum secretion) as in gingivitis is also to be considered 
in the pathogenesis of the respective diseases. These questions are 
still unsolved in their entirety though partially understood. The 
cleaning of the teeth by means of scalers, brush wheels or rubber cups 
charged with pumice and with flat floss charged with pumice is a 

1 F. H. Skinner offers the following disclosing solution : 

1$ — Iodin crystals 50 grs. 

Potassium iodid 15 grs. 

Zinc iodid 15 grs. 

Glycerin 4 drs. 

Distilled water 4 drs. 

Mix. — Put up in a glass-stoppered bottle. 

Sig. — Paint two or three teeth at a time. Rinse immediately with water. 

2 Lecture at the Philadelphia Dental College. 



750 PROPHYLAXIS 

routine method (see stains and calculus) of clearing the teeth of gross 
accumulations. At stated intervals judged by actual experience 
with the individual patient appointments are made at which any 
collections escaping the self-ministrations of the patient are to be 
removed. There can be no reasonable objection to the use of a soft 
rubber cup and oxide of tin or precipitated chalk upon the labial and 
lingual surfaces at this sitting. Following this the teeth are to be 
stained and with a wedge-shaped orangewood point and the suit- 
able abrasive, pumice, XXX silex, chalk, etc., each tooth cervix 
is polished clean in so far as the stick will do it. The use of the 
wood point has been much dilated upon and its importance exagger- 
ated to the point of abuse causing gum recession, abrasion, etc. 
In practice gentle manipulation calculated simply to remove the 
plaques is all that is necessary or desirable. It is true that it is 
better to slightly overdo the work than not to accomplish the object 
sought. All that is rational to expect is the cleansing of the buccal 
and lingual surfaces and the surfaces at the embrasures. An angle 
cured of pyorrhetic conditions should have especial attention. The 
flat floss will accomplish the balance of the work. 

The Skinner or Jack porte polisher (Fig. 619) are useful. They are 
held with the pen grasp, the third and fourth fingers being used as a 
fulcrum while the application is made by a semi-rotary movement of 
the wrist or forearm, or held with the palm grasp, the thumb being 
used as a fulcrum. 

Next flat floss is passed between the teeth and gently under the 
gum margin then bent around the neck as far as possible and drawn 
back and forth and out over the contact point. It is reintroduced 
at the same space and the operation repeated on the adjoining tooth. 
The teeth are to be reexamined for any cavities that may have reached 
a stage requiring filling, a possibility due to the difficulty of diagnosis 
at the previous sittings (see page 301). These cavity appearances are 
fewer and fewer as the sittings continue with regularity. Silver 
nitrate, 40 per cent., may be applied to any surfaces likely to decay 
as sulci or contact points or in very superficial decalcification of 
tooth cervices the saturated solution may be applied, the black stain 
resulting acting in some degree as a deterrent of further action. 

In teeth not yet fully erupted white or black copper cement or 
silver cement may be wiped into the sulci to prevent decay while they 
erupt to full occlusion. 

Any gingival irritation is noted and if necessary treated. The 
patient is cautioned as to having avoided certain points in self pro- 
phylaxis which is an all-important adjunct as plaques and carbo- 
hydrate foods are quickly collected (see page 258), 



SELF PROPHYLAXIS 751 



SELF PROPHYLAXIS. 

The theoretical ground upon which a patient is to perform self- 
prophylaxis is that plant life does not thrive if disturbed frequently, or, 
to put it in a different way, a bacterial collection or colony capable 
of caries or gingivitis production cannot get into such living and 
functional conditions as to act deleteriously if disturbed every few 
days. For example, in cane-sugar fermentation for rum production, 
the process requires much longer to start when a scoured vat is used 
than when it is left from a previous fermentation. The proper pro- 
phylaxis and even the treatment of pyorrhea proves this to be the 
case. The rationale of self -prophylaxis therefore includes: 

1. The removal of food materials after each meal. 

2. The frequent disturbance of microbic plaques mechanically or 
chemically. 

3. The neutralization of any acid formed in locations accidentally 
overlooked. 

The first two indications are partly met by the use of the tooth 
brush which should be small with fairly stiff bristles. Several good 
methods are employed. 

In one method the brush is placed with the side to the gum as in 
Fig. 694 and turned down (toward the occlusal) as in Fig. 695. 

A second to-and-fro motion over the cervices as in Fig. 696 com- 
pletes the brushing of the gum and teeth in that locality. The lingual 
of incisors are to be cleansed with the tip of the brush moved from 
side to side or with the heel of the brush as drawn out of the mouth. 
A special brush with all bristles but the end tuft (as of a "Prophy- 
lactic brush") cut away and the stubble ground down is useful for 
the lingual of incisors especially the lower when the gum has receded. 
It has also some use in bridgework as has a simple cleansing brush 
mounted in a Jack porte. Fig. 697 shows a trimmed cleansing 
brush to be mounted in a Jack porte (Fig. 619) and useful for self- 
cleansing in odd situations. 

The occlusal surfaces are to be brushed hard. Many patients 
neglect third molars through a downward or upward sweep of the 
brush, thus passing by the locality. The buccal of the upper and both 
lingual and buccal of lowers are frequently decayed for this reason. 
The lingual cervices of all molars are often overlooked. The general 
principle that if the cervices of teeth are brushed the rest will be 
cleansed is well taken. 

The second method is that of application of the bristles in a rotary 
manner, sweeping the brush about in a circle as large as the cheek 



752 



PROPHYLAXIS 



will permit and advancing in both directions. Fones 1 recommends 
very light pressure and very rapid motion over gums and teeth with 



Fig. 694 




Fig. 695 




Fig. 696 




Application of tooth brush. (Luckie.) 
Fig. 697 



Trimmed brush to be used in Jack porte, Fig. 
1 Mouth hygiene, 1916. 



SELF PROPHYLAXIS 753 

this motion upon the buccal side and a rapid to-and-fro motion over 
the entire hard palate, gums and teeth for the lingual, allowing the heel 
bristles to wipe the lingual of the incisors. 

The gum massage so applied brings blood to the tissues, inducing 
an artificial hyperemia with its nutritive, toughening effect, which 
reduces sensitivity of the tissue and increases its phagocytic power* 
thus rendering it more firmly adjacent to the teeth and resistant to 
infection. Fones also regards the gum as having a solvent power 
upon calcific granules. 

The cleansing before breakfast and at night is an additional pre- 
caution and pleasure. The brush itself should be sterilized after 
using. A good glass brush holder is sold in which a small portion of 
paraform may be placed in the lower part and is capped with a metal 
screw cap. In this the brush may remain until again needed. It has 
been shown that the ordinary brush contains one or more millions 
of bacteria after use. In health this may possibly be negligible, but 
it is irrational to reintroduce pus germs in the brush as would occur 
in pyorrhea cases. 

The Use of Floss. — The proper use of floss silk completes the fric- 
tional effort begun by the brush and dentifrice. Theoretically either 
it or a rubber band should be applied after each meal to the surfaces 
not reached by the brush. Fortunately the principle of occasional 
thorough removal of plaques is of a value quite equal to- frequent 
imperfect cleansing, yet while true it is perhaps better if patients 
habituate themselves to the use of a rubber band or floss nightly 
for the removal of food particles and plaques between the teeth. 

In practical use floss should be grasped in both hands in such a 
manner as to suspend the floss over the ends of both thumbs or on 
two fingers or a thumb and finger as a tight rope is suspended over its 
pole supports, about one inch of free floss is so stretched. The grasp 
depends upon the locality to be reached. It is to be sawed gently 
through the contacts, passed gently under one gum festoon, bent 
around the neck as far as possible and drawn back and forth as it 
passes toward and out through the contact. It is then to be 
reinserted at the same space and the adjoining tooth treated in like 
manner. Once or twice a week tooth powder or paste with slight 
grit is rubbed over the teeth and the work most carefully done, every 
surface being considered. 

As a matter of fact floss will cleanse the entire approximaj and 
two-thirds of the buccal and lingual surface if correctly used. 

The snapping of floss upon the gum and sawing into the gum should 
be avoided. The septal tissue is injured, infected, and is apt to recede; 
moreover, the cleansing is not accurately done. In case of recession of 

48 



754 



PROPHYLAXIS 



upper or lower gums there is a method of flossing by passing through 
two approximal spaces, crossing the ends and pulling on each altern- 
ately. I have had a clear case of notched lingual and approximal abra- 
sion caused within six months by this method. It was not successful 
in cleansing the actual cervix at the gum. In case of rapid formation 
of calculus this may have to be done daily. If there is any difficulty 
in the use of floss, any rough filling etc., should be made smooth at 
the contact and any overhang removed. 

Fig. 698 




Simple porte-polisher. One, shoe peg trimmed. 

The twisted wire bodkin shown in Fig. 699 is very valuable as a 
means of threading floss through a bridge space. Being readily bent 
into a half circle it returns toward the lips so as to be readily grasped. 
It should be bent in line with the flatness of the eye. To make them 
take the temper from a thin shank like that of an old Gates-Glidden 
drill, bend it into the form of a button hook; over this loop a six inch 
length of fine regulating wire. Revolve the hook in the engine and 
run the wire through the fingers of the left hand. The bodkin is run 
through any bridge space and the doubled floss used with or without 
powder or paste. 

Fig. 699 




Flexible wire bodkin slightly enlarged. 



The Use of the Wood Point or Special Brush. — That part of the tooth 
uncleansed by the floss and often uncleansed by the brush which a 
wood point or special brush will reach is the buccal and lingual cervix, 
an area which is one of the three points of inception of caries and 
gingivitis. 

A Skinner, Harrell, Jack or the author's point-holder may be used. 
The last named consists of a tube of nickelled brass, bent at one end 



SELF PROPHYLAXIS 755 

to an angle of 45 degrees (Fig. 698). It holds small shoe pegs. It 
can be used in cleansing the lingual of bridge-work. 

It is exceedingly difficult to instruct patients in the proper use 
of the wood point, but once properly instructed the results are 
little short of marvellous. In use it is to be held in the hand as 
though using the Spencerian system of penmanship. The third 
and little finger rest upon the chin or teeth as a fulcrum. The 
point is first adjusted at the distal of the third molar and with a 
rocking motion of the hand it is drawn along the cervix. The rule 
is to "keep" on the tooth but "feel" the gum. Jumping from the 
buccal of one tooth to another is to be avoided. The point should 
be deliberately but gently drawn (not rubbed), until it rests in the 
interspace. Next the fulcrum fingers are slightly shifted and the 
next tooth cleansed. 

When the anterior teeth are reached, the patient should begin 
again at the third (or last) molar of the opposite side. The motion 
is repeated upon the lingual surface. In no case should sight be 
depended upon. The sensation of contact is the best guide. As a 
means of instruction of the patient, a disclosing stain may be used. 
If desirable, the patient may occasionally use the stain as a means of 
self-instruction. The brush Fig. 697 is more readily used by patients. 

Dentifrices. — The composition of the dentifrice if not too abrasive 
seems of less value than its accurate application with the brush and 
floss. Patients who use liquid preparations only do not seem to do as 
well as those using powder or paste probably owing to a lack of 
friction. Of these preparations there are great numbers mostly 
harmless and useful. 

Pickerill has contended that antiseptics are of doubtful value and 
that ordinary alkaline dentifrices depress the flow of saliva and that, 
on the other hand, an acid dentifrice, as acid potassium tartrate in 
1 to 200 solution, increases the flow of alkaline saliva, which being 
continuous neutralizes any acid formed. As aside from a detergent 
action, alkalinity is the object sought in a dentifrice, the method 
seems rational, especially as he has found that the acid does not injure 
the teeth. 

Of his formulae the following is said to be the most agreeable: 

1$ — Potassii bitartratis (P. tartratis acidi, B. P.) . . . gr. ij 

Acidi tartarici gr. j 

Olei limonis 1U iij 

Glusidi (saccharini) gr. i 

Aquas ad fgj— M. 

The contentions of 'Pickerill are based upon his observations of 
immunes, and experiments which curiously enough do not seem to 



750 PROPHYLAXIS 

include definite experimental applications to any particular indi- 
vidual susceptible to caries. It is seemingly becoming the fashion 
to claim that prophylaxis is a failure (Pickerill admits its occasional 
value), which will not be admitted for a moment by any one who 
has conscientiously performed it each three months, or oftener, with 
reasonable assistance from the patient (see footnote page 268). Anti- 
septics are also denied a value, but even Pickerill admits their value 
in oral sepsis, so why can they be valueless in caries. They produce 
a disturbance in the medium, slight changes in which are known to 
affect bacteria, a fact taken advantage of by Pickerill as a claim for 
acid value. If disturbance of medium is of value, the frequent break- 
ing up of plaques theoretically should be of immense value and in 
practice so proves. 

Antiseptics have been shown to reduce general oral infection to 
a possible minimum when oral cleanliness is conjoined with their 
faithful use, but without exact prophylaxis cannot be depended upon. 

The writer has found phenol sodique, 1 to 7 of water, a useful 
adjunct in this connection and as an occasional germicide to 
promote the action of milder antiseptics, the following mercuric 
chloride wash used for the space of two minutes is valuable: 1 

]$ — Mercuric chlorid . gr. vj 

Thymol gr. ij 

Menthol gr. v 

Oil eucalyptus gtt. x 

Glycerin fgij 

Alcohol . . fgij 

Auqae gaultheriae q. s. ad. Oij — M. 

S. — Use as directed as mouth wash. 

Waas, by careful test, suggests that a mouth may be almost, if not 
quite sterilized for a time by the use of trichloride of iodin, 1 to 1000; 
(for formulas see page 613.) Gies 2 has agreed that soap solution, 
sodium carbonate and limewater dissolve flocculent mucin deposits but 
not the harder more adhesive collections. They should be valuable in 
dentifrices if the teeth are kept always free of old collections. 

The writer has found much value in the use of a potassium chlorate 
paste. This certainly has kept black stain from teeth which usually 
accumulated strong evidence of it within two weeks of prophylaxis, 
and caries is apparently much lessened by its use though prophy- 
laxis is a confusing factor. Potassium chlorate has been condemned 
by dentists of high standing as systemically injurious, but whether 
such small doses as might be swallowed after tooth cleansing could 
be injurious has not been scientifically shown. On the other hand 

1 C. R. Jackson, Dental Summary, 1904. 

2 Journal of Allied Dental Societies, September, 1914, p. 40S. 



SELF PROPHYLAXIS 757 

experiments 1 have been made on puppies which received thirty grams, 
daily for six weeks, were then killed and no renal lesions were found; 
the gastric mucosa showed no signs of irritation nor the blood any 
methemoglobinemia, and the animals showed normal growth. While 
large doses may have been injurious to humans this is entirely different 
from minute residue in the mouth. As a matter of fact, if the 
mouth be washed out with water no appreciable toothpaste need be 
swallowed. The alternate use of Pepsodent and Pyorrhocide, both 
well-known preparations, has also been markedly prophylactic of 
caries and pyorrhea. 

The use of chewing gum after meals has been of value in suscep- 
tibles. Either it acts by friction, removing fermentable food or by 
promoting a free flow of saliva; perhaps in both ways. 

The vigorous mastication of food stimulates the flow of saliva as 
well as cleanses the teeth. 

Whether, however, it shall be best in the future to prescribe 
a weak organic acid as a dentifrice and trust to the flow of alkaline 
saliva or use a weak alkaline wash, as lime-water one-half strength, 
or even an alkaline tooth powder or paste must be decided by actual 
clinical experiment upon susceptibles, as immunes are valueless for 
observation unless they lapse from immunity. Even here the credit 
must not be given altogether to the acid treatment side of the con- 
tention unless prophylaxis is eliminated. In brief, the whole sub- 
ject requires intelligent ventilation. We have to thank Pickerill 
and Gies, working on this line, for at least a new departure in our 
thinking regarding dentifrices. In some cases good results are 
obtained through the use at night of the milk of magnesia. It alka- 
linizes the mouth, reducing any acid accidentally formed in localities 
not reached by the brush. 

Finally a dietary should be outlined which shall be proper for 
general health, shall reduce the carbohydrate element remaining in 
the mouth (as candy and cracker consumption between meals), 
and shall induce a flow T of alkaline saliva after meals. In this con- 
nection the use of acid fruit as a stimulant to a continuous flow of 
alkaline saliva after meals and vigorous mastication for its cleansing 
and saliva stimulation are to be considered. 

The teeth should receive all needful care during pregnancy, that 
the mother should not suffer pain, but work should be of a temporary 
nature, if necessary, to avoid shock, especially at about the third 
month of gestation. Attention has been called to the fact that 
during menstruation a systemic hyperacidity exists, which can be 

1 Medical Brief, December, 1912. 



758 PROPHYLAXIS 

combated by the use of lime internally and milk of magnesia or 
lime water locally. 

In the care of the teeth during pregnancy the effect of the hydro- 
chloric acid vomitus upon the teeth should be considered, an alkaline 
wash such as lime water or bicarbonate of soda solution to be used 
after the vomiting. The same would be true of seasickness and after 
the use of any acid drug or foodstuff, such as tincture of ferric chloride 
or buttermilk in case the latter is a constant diet. (See page 263.) 

PROPHYLAXIS OF SYSTEMIC DISEASE. 

By following out prophylaxis against incipient caries the infection 
and death of pulps with the tendency to production of apical abscess 
now so common can be obviated in a large percentage of cases. This in 
turn obviates systemic infection following these conditions. The same 
is true of gingivitis. In addition if treatment of root canals become 
necessary it is important that all work should be done in the most 
complete manner possible under the conditions and under the strictest 
asepsis reinforced by antisepsis so that no septic focus shall be insti- 
tuted by operation. Teeth which show any signs of being a possible 
source of general infection through blind abscess or granuloma should 
be radiographed and either treated to a cure by all means indicated 
or extracted. Those supposedly cured should be radiographed occa- 
sionally as a prophylactic precaution and handled according to indi- 
cations. In this connection pyorrhea pockets, faulty fillings, crown 
and bridge bands and the underlying septic cement and other sources 
of sepsis of less obvious nature should be considered as possible 
foci involving systemic complications and changed to hygienic con- 
ditions. In view of these possibilities work of a nature least liable to 
induce complications should be done and those liable to produce 
them in time avoided. (See recurrence of caries, gangrene, abscess 
and pyorrhea for details. Also chapter on Infections from the 
Mouth.) 

PROPHYLAXIS OF MALOCCLUSION. 

It has been shown that general malocclusion resulting in a necessity 
for orthodontia may by suitable means be prevented from reaching 
its ultimate degree if treated early. Habits such as thumb, lip and 
tongue sucking should be corrected as soon as noticed (see page 94), 
otherwise malocclusion may occur. 

If adenoids or other nasal obstruction be a likely cause of mal- 
occlusion of this type, they should be removed early. Mechanical 



PROPHYLAXIS OF DENTITION 759 

corrections if required are purely operative and the reader is referred 
to works upon this subject. 1 

The gradual loss of teeth, especially the posteriors, frequently 
throws undue strain upon the pericementi of the remaining teeth. 
The results are overwork, pericementitis and abrasion. Proper 
support of the opposing arches is the prophylactic measure. Indi- 
vidual malocclusion or overuse, pyorrhea, etc., have to be considered 
in connection with overwork of teeth and the reader is referred to the 
chapters on these for prophylactic indications. 

In orthodontia with fixed appliances sprays are to used to remove 
fermentable particles. These are also useful in pyorrhea (for illustra- 
tion see Asepsis). 

PROPHYLAXIS OF EROSION AND ABRASION. 

In these conditions any possible local and systemic causes should 
be sought and combated and antacids used locally (see pages 200 and 
214). 

PROPHYLAXIS OF DENTITION. 

The possible causes of malnutrition possibly affecting the first or 
second dentition have been as fully discussed as present knowledge 
permits. In brief, causes should be antagonized if possible. 

It has been shown that during pregnancy osteomalacia may occur, 
and that it represents a demineralization by decalcification of the 
bones of the mother. Whether or not this may influence caries of 
enamel is not certain, though acid secretions occur from the gum 
margins, but there is no reason why the resistance of the fibrils of 
the dentin should not be lessened, or even that the dentin may not 
be to an extent demineralized, as positively claimed by some accurate 
observers (Black to the contrary). An excessive osteomalacia may 
be hela to represent a deficiency of osteogenetic nutritive material 
for the child. This would lead to an inferior development of the 
child's temporary teeth. 

Any abnormal condition of the mother should be corrected, if 
possible, in order that her general nutrition and that of the child 
may not suffer. 

Probably upon the congenital constitution of the child depends 
much of its future susceptibility or immunity to caries. 

Accepting the decalcification theory of osteomalacia, the use by 
the nursing or gravid mother of mild alkalies internally, such as a 

1 See article by J. Lowe Young, Dental Cosmos, 1917, p. 23; also Jour. Nat. Dental 
Association, August, 1917. 



760 PROPHYLAXIS 

tablespoonful of lime water repeated, and the use of lime-containing 
foods, as the cereals, and mineral waters as beverages, cannot but be 
of values as antacids furnishing a neutralizing agent for the acid, 
while the lime probably enters into the development of bone (Hare), 
and, therefore, would be useful in supplying, via the placenta, 
mother's milk, and later the child's food, the element needed for the 
development of teeth. The use of glycerophosphate of lime and soda 
has been suggested. 



CHAPTER XXVI. 
DENTAL RADIOGRAPHY. 

The great and increasing importance of radiography as a means 
of diagnosis and as an indication for therapeutics, warrants a brief 
chapter in this book. A correct diagnosis is always the first prin- 
ciple in therapeutics and may save much time, labor and chagrin. 
Roentgenology, radiology, radiography, skiology, skiagraphy, x-ray 
diagnosis to give it its various names consists in the projection of the 
x-rays discovered by Roentgen in 1896, as a part of the radiant 
emanations from a Crookes's tube through the more or less permeable 
tissues of a part of the body and thence upon a photographic plate 
or celluloid film upon which the silver in the albuminate of silver 
emulsion, coating the plate, is precipitated. Upon development in 
proper solutions this is found darkened in proportion to the amount 
of x-rays which have acted upon it. If the tissues were equally 
permeable by the x-ray the plate would be a uniform black, but as 
penetrable, impenetrable or semipenetrable substances exist together 
as instanced in the mouth by gum tissue, metal fillings, etc., and 
cancellous bone or teeth, each intercepts the light rays in different 
degree, hence the different effects upon parts of the plate produces 
a grading or a picture from which by correct interpretation informa- 
tion may be gained. 

Roentgenology also includes the application of the roentgen rays 
in the therapeutics of disease as they have a stimulant effect upon 
living cells, increasing their bactericidal powers, but in cells of low 
vitality, such as tumor cells, they can produce a desirable degenera- 
tion and necrosis while the more highly vitalized cells are merely 
stimulated. 

In the therapeutics of the more superficially located diseased tissues 
this principle has wide application. They also affect superficial 
healthy tissues unfavorably if these are " burned" acutely, or if many 
applications of shorter duration are made as in the "dermatitis" 
of operators or even their sterilization. 

There are many reasons why an operator should take his own 
radiographs, principally these (1) He knows what he wishes radio- 
graphed; (2) he obtains the radiograph without loss of more time than 

(761) 



702 DENTAL RADIOGRAPHY 

consumed in giving instruction to a radiographer; (3) the expense 
to the patient can be controlled if such is a professional consideration 
and as many radiographs taken as judged necessary and at the proper 
crisis; (4) he receives the benefit of the impression made upon the 
patient himself, a matter of importance in carrying on a treatment; 
(5) such profits as may accrue are his. 

For dental purposes the apparatus should be efficient, of simple 
construction and thus readily cared for, and so constructed as to be 
rapidly used without alarming the patient. Danger to the operator 
is usually avoided by the use of a lead screen impermeable to the rays. 
Statements of manufacturers as to the safety of lead glass are easily 
corrected by Kell's method of wrapping a film packet with wire, 
placing it in the position the operator is supposed to occupy and 
developing after a few exposures. It will probably be found that it 
has been affected as in such case will the operator be. 

The use of a lead screen is always advisable. In any case where a 
spark might jump to the patient a rubber mat should be interposed. 1 
In use no contact of the patient with any metal portion of the instru- 
ment should be allowed, e.g., the cord wheel or its connections as a 
shock may be produced. Xo shock is produced by contact with the 
adjustable arm or aluminum filter, as these are practically insulated. 

If the "soft rays" which are the non-penetrating .r-rays, irritating 
to tissue should be excluded an aluminum filter is interposed which 
intercepts them while the "hard" or penetrating rays pass on to and 
through the patient's tissues. 

The z-ray apparatus used by the operator should be operated as 
per the directions of the manufacturers as instruments differ in con- 
struction and power and are constantly changing in character. Xo 
dark-room is now required for their use. In general terms (1) the 
patient should be posed seated or standing; (2) the instrument ad- 
justed to the proper height, angle and central "focus"; (3) the tube 
flashed once to ascertain if in working order and to calm the patient ; 
(4) the packet or plate properly adjusted and the patient cautioned to 
remain quiet; (5) the exposure made and the packet, etc., removed. 

Taking the Radiograph. — Two forms of radiograph may be obtained, 
the plate and the celluloid film. In searching for wholly unknown 
conditions, for example, an impacted tooth in uncertain location, the 
plate may be better. With this method, the plate wrapped in black 
paper is placed upon one side of the face, the jaws are opened and the 
exposure made from the opposite side. The rays pass from tube to 
plate and the radiograph shows all structures in relation, but there 

1 Raper: Dental Radiography. 



TAKING THE RADIOGRAPH 763 

is apt to he superimposition of the teeth, etc., of one side upon that 
of the other. However, if the detail be sufficient, a diagnosis can be 
made or strong suspicion obtained, which can be confirmed by the 
other method of using a celluloid film, which is used in fairly suspected 
conditions. In this latter method two celluloid films, about 1J inch 
by 1| inch, with their emulsion surfaces together are wrapped in black 
paper to exclude the light and again in waxed red paper to exclude 
moisture, or the films are enclosed in unvuicanized black dental 
rubber. This covering permits the trimming of the film in the dark- 
room or box so that a better fit is obtained. The edges are then 
pinched together. 1 

The Buck "X-ograph" film has seemed to the writer to give the 
most reliable results, though others, no doubt, prefer other makes. 
This has a lead or tin and lead frame which has two films and a 
strip of black paper held within it by being stamped over their edges. 
The black paper is exposed like a picture in its frame and the metal 
backs the enclosures and is said to reflect the rays, thus intensifying 
the effect upon the film. It is readily adapted and held in the mouth. 

This packet is inserted within the mouth in proper position to 
receive the shadows of the teeth and adjacent parts. It is held by the 
finger or thumb of the patient, the rest of the hand being kept out 
of range of the .r-rays passing to the negative. The correct angle 
of the rays having been previously determined, the exposure is made 
for a predetermined number of seconds. The small intraoral radio- 
graph gives greater detail of the area under consideration and is 
usually employed. From three to five teeth may be radiographed 
on one film, the most important being centered. For an entire mouth 
usually ten serial radiographs are taken. If the patient gag, as occa- 
sionally occurs, a solution of novocain may be painted on the mucous 
membrane. Radiographs are usually mounted on a convenient card 
having apertures covered with opalescent celluloid, permitting the 
transmission of a soft light for examination. These cards usually 
have descriptive printing, identifying the part of the mouth radio- 
graphed, or it may be written on the card. Examination is made by 
holding the film, mounted or not toward the strong daylight or in 
front of an electric bulb. 

The Angle of the Rays. — Owing to the conformation of the hard 
palate in order to obtain a corresponding length of an upper tooth 
and its radiograph, an angle of about 45 degrees with the tube center 
to the axis of the root should be observed well toward the apex. An 
angle of 90 degrees or more lengthens the tooth in the radiograph. 

1 Kells: Johnson's Operative Dentistry. 



704 DENTAL RADIOGRAPHY 

111 the lower jaw from cuspid to cuspid an angle of about 120 degrees 
to the axis of the tooth is necessary owing to the inclination of the 
film toward the lingual. The lower bicuspid and molars may be taken 
at about 90 degrees. Kells suggests that the angle be determined at 
the chair and a spot made on the face with a blue pencil as a focal 
spot for the .T-rays. 

These angles may be changed to obtain certain details. For 
example, it may be more important to obtain details of the apical 
regions of an upper molar than the exact root length. 

Radiographs should be taken at opposite angles in upper first 
bicuspid or molars as the two roots may superimpose. their shadows. 
The length of exposure should be measured in seconds by the watch 
or a count at about known speed and varies from one to ten seconds 
according to apparatus, density of tissues and details desired. With ■ 
an apparatus having the aluminum filter, even sixty seconds are safe, 
but unnecessary. An Eastman standard film requires three seconds. 
The Buck about the same, though the "speed" packets require less. 
To identify the films pencil the name and the location radiographed 
on the paper wrapper or imprint it with pencil on the metal casing. 

Developing the Radiograph. — The operator may prefer his own 
solutions but the developing and hypo solutions sold as Eastman's 
are satisfactory and convenient, when made up according to direc- 
tions. To develop, say a half dozen or more negatives the writer 
proceeds as follows : The films in their wrappers are laid in a pile in 
the center of the top of the developing "dark box" and the watch 
laid in full view. The proper cups are filled, two with developer, 
two with hypo and one with tap water, all should be below 65° F., 
and in hot weather be chilled by placing in a pan containing ice-water. 
Each should be in a customary position. 

An open knife and a cloth or sponge should be placed within and 
the light excluded by closing the aperture, permitting the sleeves to 
be exposed. Introduce the left hand, holding one Buck film and a 
discarded Eastman or other black paper wrapper. (The extra 
wrapper is not necessary when using paper-wrapped packets.) 
Insert the right hand and grasp the knife and with the blade, peel 
up one end of the metal casing and rip out the enclosures; put one 
film between the fingers and the casing in the palm of the left hand and 
wrap up the remaining film and black paper in the black paper and 
put it with the casing; place the film to be developed into the devel- 
oper, add the minutes required (about seven) to the time on the watch, 
withdraw the left hand, place the packet and casing on top of the box 
over the cup containing the film. Take up another packet and paper 
and repeat the process, but putting the film into the other developer 



INTERPRETATION OF RADIOGRAPH* 765 

cup. Withdraw both hands and pencil the time of expiration of devel- 
oping upon bits of paper. Utilize the time elapsing to enclose each 
undeveloped film in an additional red paper. Just before the expira- 
tion of the time, introduce the hands and prepare a third film, holding 
it ready in the left hand. Remove film No. 1 from the developer, wash 
in the water and put into the "hypo" and put film No. 3 in its place 
in the unoccupied developer. Withdraw the left hand, place the 
packets over film No. 3 and remove the packets of film No. 1 to posi- 
tion over the hypo. Take up film No. 4 and insert, prepare, remove 
No. 2 to corresponding "hypo," put No. 4 in its place, put the packets 
in corresponding position on top of box. In five minutes remove 
No. 1 from the hypo as follows: Jig. loose from the side of the cup, 
pick up by the edge between forefinger and middle finger and let fall 
gently into the palm of the left hand, but prevent contact by holding 
the edges with the palmar sides of the fingers. Hold the hand rigid 
and withdraw, take up film by the edge with a spring clip, examine 
by electric light, but do not let the gelatin be melted, wave through 
water in a bowl, hang on the edge of the bowl with the extra film and 
casing clipped against the outside of the bowl. Repeat with No. 2. 
The hypo cups are now free for introduction of Nos. 3 and 4 at the 
proper time (about a minute later) and Nos. 5 and 6 can be introduced. 
Between handlings the fingers should be wiped off. The films should 
remain in the water at least a half hour, but may remain the rest of 
the day. Too long immersion may cause the solution of the gelatin 
and much chagrin ; about twelve films may be developed in an hour. 
The extra films are not developed unless something goes wrong or 
unless duplicates are required, in the latter case two films are devel- 
oped at once, back to back. Plates require dark-room facilities and • 
may be developed under an orange light and washed in running water 
after "fixing" in hypo. They might be done in the trays furnished. 
After a proper time in water the films are to be hung on a large cord, 
as a double electric light cord, with their corresponding packets, or 
on the edge of a dry bowl and allowed to dry. They are then mounted 
and described on the mount or put into small envelopes with a descrip- 
tion. By this system the operator identifies each film throughout 
without mental effort. 

The use of paper wrapped films differs but slightly and this and 
other modifications will suggest themselves. The technic may easily 
be carried out and even the radiograph taken by an easily trained 
assistant though this latter is best done by the operator. 

Interpretation of Radiographs. — Having been taken for this purpose 
interpretation is all-important, and while obvious conditions are 
susceptible of correct interpretation by a radiographer, a clinical 



766 



DENTAL RADIOGRAPHY 



knowledge of the case is required in many cases. Therefore, final 
judgment is best passed by one having facilities for digital, electrical 
and other means of diagnosis at hand. When a diagnosis rests upon 
the question of vitality or non-vitality of a pulp, and the facts are 
not proved in any way by the radiograph, one should apply the tests 
described on page 493. 

In studying the details it must be remembered that the .r-rays 
penetrate and pass through all substances about the mouth, except 
metals and certain root canal fillings, such as gutta-percha, and pastes 
containing bismuth. It completely penetrates cotton which therefore 
does not "show" (Fig. 700). 

Fig. 700 




Wire wound with cotton in bicuspid. Case of old vital pulp stump, perforation 

suspected. 

In the degree in which it passes without interception, tissues and 
substances are "radiolucent" (radiolucency) otherwise they are 
" radiopaque" (radiopacity) (Ottolengui). The gum, medullary 
tissue, mucous membrane and space in the antrum, pulp cavity and 
the pericemental tract are all so highly radiolucent, that the silver in 
the negative is heavily precipitated and blackened. They show dis- 
tinctly, however, in contrast with juxtaposed tissues, which intercept 
the light in some degree. Areas of resorbed bone or root and abscess 
tracts show dark in the negative as they are areas of soft tissue like 
pericementum. The trabecular of bone, the more cortical bone, the 
root substance, porcelain, the enamel and some root fillings, as 
cement, are semi-radiolucent and, having intercepted some light, 
show grayish in the negative. Finally metals, gutta-percha and root 
fillings with bismuth practically intercept all the rays and show as 
white in the negative (film), the silver not being precipitated. In 
a positive picture all these are reversed if shown at all. With these 
facts and the anatomy of the parts known, and with the clinical 
experience and applied tests one using common sense, may arrive at 
a diagnosis often at once. Certainly after investigation. 

Certain facts should be stated. (From appearance in the negative 
the opposite of the illustrations.) 

The angle of exposure for upper teeth often superimposes the light 



INTERPRETATION OF RADIOGRAPHS 



767 



outlines of the antrum upon the radiograph of the teeth. This is normal 
though often confusing (Fig. 701). An apical abscess or granuloma 





Fig. 701 






4; 


k 




% 


v . 

m 






f . 


i 





Fig. 702 




on the teeth superimposed will show as a dark area within this out- 
line. In case of doubt test for pulp vitality. In one case an oral 
surgeon questioned the vitality of a L. S. 2 B. which after perforation 



Fig. 703 



Fig. 704 



rtTl 



r m 



*<**• 




of a gold crown demonstrated vitality by sensitivity of dentin. The 
nasal cavity occasionally is taken in a radiograph, but must not be 
mistaken for a necrosis (Fig. 703). 



Fig. 705 



Fig. 706 




V 



%/» 



The normal cancellated bone shows as a lattice work, the cortical 
bone (lamina dura of the alveolar socket), as a more solid, grayish- 



768 



DENTAL RADIOGRAPHY 



white line or area (Figs. 711 and 712), occasionally owing to a degree 
of osteoporosity or perhaps osteoclasia, the bone will have an indefi- 
nite dark area somewhat suggestive of abscess area. While it should 
be carefully considered it may generally be excluded owing to vitality 
of the teeth, though in case of pain about the tooth, non-septic peri- 
cementitis or pericemental abscess (with bone resorption) may be 
considered (Figs. 568 and 569). 

The gums are often not shown; rarely a faint outline is seen. The 
molar in Fig. 706 was well covered with gum tissue. The perice- 
mental outline is black, normally it is a narrow strip between grayish 
white bone and more gray root structure (Fig. 705). The root is 
clearly outlined in good pictures, sometimes they are radiolucent and 
may seem absorbed, in which case another picture should be taken, 
or careful interior exploration should be done. 



Fig. 707 



Fig. 708 





Upper molars often seem to show but one root, a better radio- 
graph at a different angle or from above is indicated (Figs. 704, 705, 
and 707). Root canals show plainly in some cases in others equally 
good canals do not show. (Fig. 708.) This depends upon their 
being more radiolucent than the rest of the root. Their contents 
show when radiopaque. Broaches show plainly, but may show as if 
in line with a canal, yet be out of line labiolingually. Protruding 
broaches and canal fillings are shown (Fig. 709). Diagnostic wires 
are shown as in Fig. 409. 

A canal may appear as though filled, while an instrument can be 
passed to one side; this is due to a single cone not having been 
thoroughly packed, occasionally this space shows distinctly. 

Secondary dentin and pulp nodules usually show as constrictions 
of the pulp chamber or foreign bodies therein (Fig. 349). Sometimes 
they do not show at all. Cavities are sometimes noted, as in Fig. 708. 

Calcific pulp degenerations do not show well as a rule. Perfora- 
tions show as a rule, as in Fig. 70S. Hypercementosis is well defined, 
as a rule as a root enlargement.- (Figs. 551 and 554.) 

Resorptions may be seen or inferred or be masked if covered up 
by more labial structure (Figs. 514, 522, 562 and 709). 



INTERPRETATION OF RADIOGRAPHS 



709 



Incipient pericementitis is more readily diagnosed by symptoms 
and a strong transmitted light, but abscesses on apices or granu- 
lomas, or perforations show dark areas in the negative. Granu- 
lomas are shown as sac-like bodies enclosed in a bony cell (Fig. 538) . 

Pyorrhea pockets and lateral resorptions of bone show as though 
the pericemental tract were enlarged. Confirmation by instrumental 
examination should settle the diagnosis (Figs. 632 and 637). Perice- 



Fig. 709 



Fig. 710 





mental abscess may show a dark area alongside a root. Fillings may 
appear as though near or into a pulp cavity. This may be due to 
superimposition in the picture as when a small buccal filling appears 
to lie in a pulp cavity, but is merely between it and the x-rays. 
The relations of deciduous and permanent teeth are usually distinctly 
shown as are impacted teeth, supernumeraries or the absence of tooth 
germs (Figs. 710 and 711). The condition of the root foramen is 
also visible (Fig. 710). 



Fig. 711 



Fig. 712 




^m 



Imbedded roots are seen as in Fig. 307. 

The gums may be healed over. 

Fractures of roots can be noted as in Figs. 249 and 483 as can 
fracture of the jaw. The mental foramen may be confused with 
abscess (Fig. 475). 
49 



770 DENTAL RADIOGRAPHY 

There are many radiographs shown throughout this book which 
will further illustrate interpretation. 

It may, in brief, be stated that whenever a condition exists or is 
suspected in which a differentiation of objects may be looked for, 
the radiograph will be of use. 

There are numerous details connected with the subject of radiol- 
ogy which if they have not been touched upon in this chapter 
or in place in this book may be found in various text-books of 
great value. Notably Raper's Dental Radiography, Kell's chapter on 
the ' 'Application of the Rontgen Ray in Dentistry" in Johnson's 
Text-book of Operative Dentistry and Ivy's Interpretation of X-ray 
Films. The idea here is to give a few important principles useful to 
those who make their own radiographs or diagnose from those of 
other radiographers. 



CHAPTER XXVII. 
APICOECTOMY AND ROOT AMPUTATION. 

Apicoectomy or apexotomy may be defined as the surgical removal 
of the root apex, and is a partial root amputation or resection. 

Root amputation, while including apicoectomy, might specifically 
be defined as the removal of an entire root at its junction with the 
crown, and can be performed only on a multirooted tooth. The object 
of these operations is to save a tooth from extraction by removing a 
part or all of a root so diseased as to be otherwise incurable, including 
in this protruding broaches irritating root fillings and inaccessible 
perforations all of which have led or may lead to untoward disease. 
It has been suggested that all roots not capable of filling to the end 
should be immediately apicoected. The writer does not believe this 
practical largely because patients will not submit, but there can be 
no surgical objection. 

For the same reason many prefer extraction to any amputation 
and in view of the total uncertainty of root canal treatment it would 
seem that extraction and bridge or plate work in most cases of root 
disease not amenable to careful treatment is often the advisable 
procedure. 

The operation has been objected to in toto by some prominent 
dentists which seems equally irrational. The operation therefore 
seemed limited by the following considerations: 

1. The necessity for its employment as a means to a cure. 

2. The feasibility in consideration of the location of the root in 
question. 

3. The willingness of the patient to prefer the operation to a sub- 
stitute tooth. 

The conditions favoring apicoectomy are: 

1. Incurable apical abscess or granuloma or cysts including apical 
perforations protruding broaches or root filling, etc. 

2. Curved or inoperable root ends with probable delta-like 
foramina. 

3. Limited apical hypercementosis. 

4. Limited apical root resorption. All these in locations reason- 
ably operable in case of teeth otherwise not involved. 

The conditions favoring root amputations are: 

(771) 



772 APICOECTOMY AND ROOT AMPUTATION 

1. Advanced pyorrhea involving or closely approaching the apex, 
especially when the rocking of the tooth draws the root out of its 
socket and returns it to place. 

2. Apical abscess discharging along the root at the gum margin 
which finally is about the same as Class 1. 

3. Perforations in the gingival third of the root not amenable to 
treatment or preventing proper treatment of the apical portion of the 
root. 

If all considerations indicate the operation of apicoectomy the 
root canal should be sterilized at least as far as the intended excision 
by formalin or other applications repeated daily until sterility of the 
root interior is assured or Howe's treatment may be used. The 
root is then filled under strictly aseptic precaution with solidly 
packed gutta-percha points using either eucalyptol, oil of cajuput, 
xylol or a xylol solution of gutta-percha or chloropercha as a 
solvent in very small quantity merely moistening the root. Prinz 1 
prefers a thin zinc chlorid cement followed by a cone of gutta- 
percha as rendering disturbance of the cone less likely. It does 
not matter if the filling pass through the apical opening or perforation. 
Any remaining roots are of course properly filled. The root is now^ 
ready for the surgical procedure if any remaining roots are deter- 
mined to be in good condition. In root amputation the remaining 
roots are treated and filled but the root to be excised need not be 
filled except to the point of excision. The bulb of the pulp cavity 
must be. filled in this case. A good radiograph is obtained if not 
already done, so that one may be guided by it. 

The Operation of Apicoectomy. — Asepsis and anesthesia are first 
secured (see respective chapters) . The technic of this operation differs 
with different operators and depends somewhat upon whether the 
apex is solidly embedded in bone as in an apicoectomy for prevention 
of future apical abscess (condition 2 on page 721) or whether an area 
of bone has been removed from about the apex by disease leaving the 
apex practically free. 

For the first condition Levy's operation seems desirable. 

1. A liberal semilunar cut is made having its apex a little occlusally 
to the point of the desired resection and the flap including the peri- 
osteum dissected free. 

2. With a round bur the bone is removed from over the root at this 
point and with a sharp pointed dentate fissure bur the root apex is 
severed, the cut sloping obliquely apexward from buccal to lingual 
to give leverage for an elevator (the reverse if operating lingually). 

i Dental Cosmos, May, 1918, p. 386 r 



THE OPERATION OF APICOECTOMY 773 

3. With the round bur the bone is now removed from over the 
apical portion creating a path for the root to escape. 

4. With a proper elevator inserted in the oblique cut the root apex 
is forced buccally. 

5. If a granuloma, etc., exist the parts are thoroughly curetted, 
the remaining root end shaped and smoothed and the flap stitched or 
the cavity packed or a clot merely induced without stitching accord- 
ing to indications When a root apex lies free either Levy's technic 
may be employed or that in more general use. 

1. The lip or cheek is held back by a retractor in the hand of an 
assistant. A semilunar cut is made with apex crownward and well 
below the point of resection chosen but not too near the gum margin 
as necrosis of this may occur. Any fistula is included in it. 

2. The flap including the periosteum is freely dissected back with 
a periosteal elevator and held with a pronged retractor. 

3. Any bone obstructing the path of operation is removed with 
pointed fissure or round burs, though chisel and mallet are preferred- 
by some. There is no advantage visible in chisels and a number of 
disadvantages. 

4. A point of healthy root and pericementum is selected and the 
root end cut off with a flat or oblique cut according to the necessity 
for elevation from its bed. The writer can see no advantage in merely 
curetting the root end without amputation except in case an acute 
apical abscess in the third stage be lanced under anesthesia and a 
chance to curette offer. The conditions indicating the surgical open- 
ing of the gum usually demand apicoectomy except of course when 
merely done to establish an artificial fistula. 

5. The root is dislodged or lifted out with pliers or if it escape into 
the abscess cavity is removed with the curette (Fig. 713). 

6. The necrotic tissue lining the abscess cavity is removed with the 
curette and the bone thoroughly scraped or burred to tissue capable 
of granulation and the root end smoothed and rounded with sterile 
finishing burs or stones. 

7. The treatment of the abscess cavity varies. The usual method 
is to thoroughly wash it out with boiled physiologic salt solution or 
mild antiseptics. Next to draw sufficient blood to make a clot filling 
the cavity and then stitch the wound with sterile horsehair. A curved 
needle and forceps for using the same are necessary for this. 

The mouth should be kept as sterile as possible. Prinz has recently 
shown that the flap can be pressed into place and kept in apposition 
by a pad of gauze containing an antiseptic solution. The blood will 
coagulate and hold it in position. 



774 



APICOECTOMY AND ROOT AMPUTATION 



Fig. 713 



Fig. 715 




Portion of root and canal filling lying 
in abscess cavity after apecoectomy. 



Fig. 714 






Friedman's curettes for oral surgery. 






0) 
-4 



Stellite combination knife and periosteal 
elevator. (Prinz, Dental Cosmos.) 



RESULTS OF MODIFICATIONS 775 

Buckley suggests a gauze packing saturated in euroform paste as 
a protective, stimulant, antiseptic and analgesic. After twenty-four 
hours it is removed and bismuth bone paste injected every few days 
until the cavity is filled with healthy granulations. This would be 
of greater value in large abscess cases; but a blood clot is the best 
occupant of a cavity about the alveolar process, as Nature shows 
after extractions. 

Modifications. — Buckley 1 adopts Schamberg s technic in that he 
makes a vertical incision, dissects the periosteum and flaps to each 
side and retracts with his special retractor a pair of pronged 
retractors attached to a sliding telescoped bar. The spring auto- 
matically holds the lips of the opening apart. He also prefers the 
mallet and chisel. 

Results. — As recently performed the results are satisfactory in 
nearly all cases. The parts heal without pus formation though 
should such occur, the part may be irrigated daily with Dakin's 
solution or even bone paste injected. 

Granulations gradually replace the clot and bone gradually replaces 
these. (See Figs. 528 529 and 530.) 

The points to avoid are: 

1. Any septic contamination. 

2. Oversaturation with adrenalin, etc. 

3. Curetting into the apical regions of other teeth or cutting their 
sides. 

4. Insufficient curetting of the walls of the abscess cavity. 

5. The loss of the root end. 

6. The use of hydrogen dioxid. 

7. After sepsis of the mouth. 

8. In posterior teeth other important parts as the antrum. If this 
be entered it is left to care for itself any blood discharging via the 
nose. One should not open into the antrum except by accident during 
the curettement as in the amputation one should keep at a lower level. 
Also one should recognize the fact at once and desist unless the case 
is originally one of antral empyema, when a larger opening removing 
all dead bone should be made and the case treated as antral (see 
page 551). 

Cysts in apicoectomy cases are treated as are granulomas with 
the additional care not to enter other cavities or injure arteries, etc. 
They are packed with gauze, repeated after twenty-four hours and 
again every three or four days thereafter until the cavity is lined 

1 Text-book of Dental Materia Medica, and Therapeutics, 4th ed. 



776 APICOECTOMY AND ROOT AMPUTATION 

with epithelium. After a few packings bone paste may be introduced. 
Prinz 1 gives the following directions: 

If — Yellow wax 4 drams 

Cottonseed oil ' 14 "• 

Aristol 1 " 

"Melt the wax and oil in a porcelain capsule on a water-bath, let cool, remelt and add 
the aristol, remelt once or twice until a perfect mixture is obtained." 

"The cavity is dried, painted with a mixture of tincture of iodin 
2 parts, acetone 4 parts and coated with a thin film of sterile paraffin 
oil. The bone wax is melted by heating the bottle in very hot water 
and 'poured in' the patient being posed in accordance with gravity. 

When loosened it may be removed and when the cavity is well 
lined with epithelium the patient may be instructed to wash the cavity 
with warm salt water by means of a soft rubber ulcer syringe." 

ROOT AMPUTATION. 

The operation of removing a root at the bifurcation is quite 
simple in case the particular root is loose from pyorrhea (see page 
772), but the removal of a solidly placed root is very difficult unless 
a surgical path for it is made. Indeed, there would seem to be no 
particular use for the operation when the root is firm except in case 
of a perforation in the coronal or middle third. In such a case it is 
best to make a vertical cut over the bone, dissect back either flap 
with a periosteal elevator and remove the bone liberally from over 
the root. Make an oblique excision of the root near the neck so as 
to favor the use of an elevator, brace the tooth with the fingers or 
opposite teeth and apply the force. If necessary modelling compound 
may be adapted over the tooth (exposing the root freely) , the finger 
or opposing teeth to act as a brace. The oblique cut is smoothed up 
later, no sharp splinters should be left to irritate. They are apt to 
form as the tooth and root part. If desired the face of this root may 
be veneered with amalgam to be polished later. 

The diseased area is to be curetted and a clot drawn and the 
mouth kept as sterile as possible. If thought best steresol may be 
painted over the dried part (see page 131). 

1 Dental Cosmos, May, 1918. 



CHAPTER XXVIII. 
PLANTATION OF TEETH. 

By plantation is meant the more or less forcible placement of a 
tooth or appliance to carry one in a natural or prepared alveolus. 

There are three varieties: 

Replantation consists in the return of a tooth to its more or less 
natural alveolus. 

Transplantation is the plantation of a foreign tooth in a natural 
or modified alveolus from which naturally a root has been recently 
extracted. 

Implantation is the plantation of a foreign tooth or root or of an 
artificial root into an alveolus specially prepared for its reception in 
the alveolar bone. 

REPLANTATION. 

As above defined this is a very old operation and still a recog- 
nized method of procedure which is indicated under the following 
circumstances : 

1. When by reason of an accident such as a blow, fall or accident 
in extraction the tooth is forced out. 

2. When it is considered preferable to apicoectomy or root ampu- 
tation as a means of curing an otherwise incurable abscess, perfora- 
tion, etc. 

The first indication has even been acted upon by parents who have 
quickly pressed teeth into their places where they became reattached. 
Reattachment of the pulp has even occurred. 1 At the present time 
an operation of this kind could only be admissible when teeth are 
but partially removed in which case Dakin's or other solutions should 
be used to irrigate the parts before returning the tooth to place and 
later if pulp death occur the pulp should be removed, etc. 

When the tooth is out it is often found that there is no fracture of 
the alveolar bone, the tooth having sprung out owing to the inclined 
root and alveolar surfaces as occurs in elevating in extraction. The 
tooth crown may, however, be broken and may be restored or any 
cavities filled or a new crown arranged. Its pulp should be removed 
and the canal filled to the end with gutta-percha; asepsis must be 
observed in this. 

1 See page 367. 

(777) 



778 PLANTATION OF TEETH 

Some prefer to further fill the root end with a small cohesive gold 
filling or a portion of gold screw. The writer prefers the gutta- 
percha. The root canal may be entered from the apex with Gates- 
Glidden drills or from the crown later using the drills. 

The tooth is to be placed in an antiseptic solution for aseptic reasons 
and to preserve the color, for dried teeth change color permanently. 

If necessary local anesthesia is resorted to. The mouth is made 
as aseptic as possible and the parts thoroughly so (see chapter on 
Asepsis). Any clot is swept out and the tooth tried in place. If 
it does not go to place the socket should be slightly reamed and 
washed out with a mild antiseptic and the tooth planted. Kells 1 
suggests that a crystal of resorcin be placed on the root end just before 
planting. I have usually used diluted phenol sodique 1 : 6. If there be 
difficulty in placing the tooth, the patient may bite upon it. An 
impression is now taken in modelling composition which need not go 
much to the labial so as not to reextract the tooth. A splint of 30 
gauge pure gold or 33 to 36 gauge 22K gold is struck from a zinc die to 
cover the linguo-incisal two-thirds and the labio-incisal fourth of three 
teeth. This is cemented over the teeth after careful adaptation and 
should remain for from six to eight weeks, as a rule, when it can be 
sprung off and, if the tooth be not firm, replaced. Hydrogen dioxid 
should be freely used by the patient and he may use a 25 per cent, 
solution of Talbot's iodoglycerol as a lotion 2 over the parts twice 
daily. Frequent inspection and prophylaxis are advisable. 

Replantation for Disease. — The choice between apicoectomy (or 
root amputation) and replantation depends upon the feasibility of 
the former and the state of disease. Perforations in the cervical 
half of the root indicate the latter. Multirooted teeth with granu- 
lomas might better often be replanted if replantation is not also 
contra-indicated. The disease and the indication ' are seldom co- 
existent; but this does not of necessity limit an operator's range if 
opportunity occur. 

The writer has usually preferred to extract and cut off the necrotic 
root end and await a healing process before replantation in abscess 
cases as being less dangerous than immediate work and leaving the 
root end. 

The procedure of cutting off the root end removes a necrotic and 
often septic area if apical abscess was the reason for removal, and 
while the present thorough aseptic curettement of the abscess tract 
may render the operation of immediate replacement safer than 
formerly the writer has in mind an unpublished case of a former 

1 Johnson's Text Book of Operative Dentistry. 

2 See Chapter on Asepsis. 



IMPLANTATION 



779 



prominent Philadelphia dentist whose patient died as the result. To 
be sure the times were preaseptic. The condition of a septic alveolus 
seems to require delay if only for the purpose of reducing the sepsis. 
In a case of lateral perforation as a cause the root end is not removed. 
With these differences of view conceded the other procedures are the 
same. 



Fig. 716 



Fig. 717 





Replantation case lost after about two 
months. 



Implantation done in the early days 
of the operation, lost after about two 
years. 



1. Before extraction an impression is taken and a splint con- 
structed and kept sterilized. 

2. The tooth is extracted with effort to avoid cervical injury and 
placed in an antiseptic (and with the apex cut off), the root canal 
reamed, sterilized and filled ; any lateral perforation reamed into a 
cavity with parallel edges and solidly filled with amalgam and then 
polished. The tooth is again put into the solution until needed 
and the operation performed at leisure. 



TRANSPLANTATION. 

This is also an old operation. It does not differ materially from 
replantation except that it was formerly done freshly, septically, and 
hence could be a cause of disease by transmission or by ordinary 
sepsis. At present the difference lies in the fact that the alveolus 
is simply made to fit the root prepared as for replantation. Asepsis 
renders the question of disease negligible. The splint would be made 
as in implantation. 

IMPLANTATION. 

An impression and bite are taken and " set up." A hole is bored in 
the plaster cast where the alveolar process will be reamed and a proper 
extracted tooth which has been kept in alcohol and glycerin is selected 
and its root prepared as for replantation except that the apex should 



7S0 



PLANTATION OF TEETH 



not be removed, but if roughened at the apex may be smoothed. In 
default of a tooth a good root is used and a crown mounted perfectly 
upon it, using the cast and bite as a guide to occlusion, fit and direc- 
tion of root. The tooth is " tacked" in place with wax or plaster 
on the labial side and the splint constructed as for replantation. 
Tooth and splint are placed in an antiseptic until needed. 

At operation anesthesia is secured. A trephine has its collar set 
at the level of the point to which the root neck enters the bone while 
the edge of the trephine is just short of the root apex if smaller 
than the trephine at it if larger. The bone reamer is set likewise, 
all being handled aseptically. (See Figs. 718 and 720.) The area 
of operation is isolated and thoroughly asepticized. With a surgical 
knife a mesiodistal incision is made just lingual to the center of 



Fig. 718 



Fig. 719 



Fig. 720 



o ooOO 





12 3 4 5 

Younger-Walker trephines. 



1 2 

Ottofy spiral crib knife. 




Ottolengui's reamers. 



the proposed entrance point, a second buccolingually at right angle 
to it is made distal to the entrance point and a third mesial to 
it, each reaching the bone. With a periosteal elevator the gum is 
dissected up. The trephine is carefully but powerfully driven by 
the engine into the alveolar bone observing the intended direction. 
When in to the collar the bone reamer is used to enlarge the socket. 
The tooth is tried in and the socket altered as needed. The trials 
and alterations are continued until the tooth is in good position and 
preferably quite tight. The splint is tried on and burnished as needed. 
All being ready, the tooth is dipped in phenol sodique 1 to 6 and the 
socket washed out. A little blood is invited and the tooth put in, the 
parts dried and the splint set. The splint should remain about eight 
weeks, when it is to be removed and the attachment tested. Strict 
asepsis and prophylaxis are valuable aids to success. This operation 



IMPLANTATION 



781 



is only indicated for a single anterior tooth when there is sufficient 
alveolar bone and when it is preferred by both operator and patient 
to bridge work. 



Fig. 721 




Fig. 722 



K/tXW? 



•• 



Fig. 723 



m 




III 



Tubular knife for 
cutting gum. 



Trephine with central 
starter later removed. 



Trephine with central 
starter removed. 



Fig. 724 



Fig. 725 



Fig. 726 



Fig. 727 





Artificial socket Artificial root and 

drilled in bone, a crown separated, 
core being left. 




Artificial root 
with crown in 
place. 



Artificial root in 
place. 



If the operation does not fail practically at once from a few years to 
sixteen years may be hoped for. These conditions render the opera- 
tion infrequent but it has its place (Figs. 716 and 717). If sepsis 
occur the patient may complain of a bad taste. This will probably 
be due to a loosening of the splint. 

Greenfield 1 has introduced an artificial root made cribriform of 



i Pental Cosmos, April, 1913. 



782 PLANTATION OF TEETH 

platinum soldered with pure gold. Special instruments of varied 
sizes are necessary to correspond with the sizes of the roots. Under 
due aseptic precaution the gum is cut with a tubular knife, and the 
socket drilled with a circular trephine, which preserves a core of 
bone, and the root covered with Beck's bismuth paste is inserted. 
Later a crown is mounted or a bridge attachment constructed. 
The reader is referred to the article for details. The editor has had 

Ik 

no experience with this method. All other artificial roots are said 
to be failures. 



CHAPTER XXIX. 

THE USES OF ELECTRICITY IN DENTAL 
THERAPEUTICS. 

Electricity is used in dentistry in one of the following ways, 
each of which contributes to the care of the teeth and their diseases, 
according to its use: 

1. As a source of mechanical power, heat or light. 

2. As a means of mechanical or electrical vibration of tissue or 
cells or possibly as a chemical alterative to cells. 

3. As a means of introduction of medicaments bodily into tissues 
(cataphoresis, anaphoresis) . 

4. As a means of electrolytic decomposition of chemicals for the 
introduction of the selected ions into the tissues. 

5. As an agent acting in place of an anesthetic by substituting a 
continuous bearable sensation. 

6. As a method of testing pulp vitality or death. 

7. As a sterilizing or bleaching agent. 

1. Power. — The uses of electricity as a means of actuating electric 
motors which either directly from the armature shaft or by means 
of pulleys and cords, drive fans, dental engines, lathes, air com- 
pressors, etc., is so familiar that one need but mention them. These 
employ either of the commercial currents, the direct or the alternating, 
usually in their full voltage and connected directly to the apparatus 
from the electric light plugs or transmitted through special full- 
voltage connections on a switchboard where they are conveniently 
controlled. These derive power through the alternate making and 
unmaking of temporary magnets which attracts the armature up 
to a certain point and then another takes up the work, thus rotary 
motion is obtained. Power is also obtained by the use of the prin- 
ciple of attraction of a hinged armature by a temporary magnet. 
The latter consists of a core of soft iron wound with insulated wire 
through which current passes, when the circuit is completed by the 
contact of the armature at the time it is separated from the magnet 
by a spring which pushes or draws it back. At this instant the 
current passing through the wire induces a current in the iron core 
thus making it a magnet. It attracts the armature (overcoming the 

(783) 



784 USES OF ELECTRICITY IN DENTAL THERAPEUTICS 

power of the spring) which flies toward it thus breaking the electric 
connection. The magnet loses its temporary power, the spring 
forces the armature back again. Electric connection is renewed. 
Thus vibratory motion is produced. 

The electric telegraph, telephone, spring-battery interrupters, 
electric bells and other devices are thus operated and rotary devices 
like motors are but a modification of the principle. 

The electric mallet uses the impulse of the armature when attracted 
to the magnet causing it to strike the plugger handle or corresponding 
device. An electrically operated vibrator for massage or therapeutic 
vibration utilizes the power of the armature when drawn back by the 
recoil of the spring though it can be operated as in the electric mallet. 

Heat. — This is obtained by the passage of current through wire 
which by its resistance to the current becomes heated while it con- 
tinues to conduct current because its melting-point is high. When 
this is exceeded the instrument " burns out." The cautery is used 
for the purpose of burning or carbonizing tissue, the removal of which 
is desired (see page 111). The root drier for removing moisture from 
root canals and dentin has its point heated at one end by a current 
heating its socket in a manner similar to the cautery. The gutta- 
percha heater carries and softens gutta-percha pellets for filling pur- 
poses or can be used to supply heat for diagnostic purposes (see page 
483). The hot air syringe for drying about cavities, roots, etc., even 
to dessication if required has a coil of wire similarly heated and over 
which air from the compressor tank passes. 

In all small devices platinum wire is used and special resistances 
are supplied on the switchboard to control accurately the quantity 
of cm-rent in order to prevent "burning out." In the gold annealer 
and the electric oven the platinum wire is embedded in fire clay 
which it raises to a high heat. In electric water heaters or electric 
sterilizers, other metals as German silver may be used and special 
replaceable "fuses" melting at lower temperatures are. usually fur- 
nished as safety devices to protect the wiring. 

Light. — Light is required as in the ordinary room lighting and 
oral lighting and for diagnostic purposes as in the antrum lamp and 
dental diagnostic mouth lamp (see page 302). The principle involved 
is the passage of current through a special filament (carbon, tungsten, 
etc.), in a vacuum or nitrogen filled glass bulb for the purpose of 
preventing access of oxygen which would allow immediate destruc- 
tion of the filament. It is a question of heating to incandescence, 
thus producing light. 

Specially colored bulbs, violet, blue, etc., as well as white are con- 
sidered to produce chemical effects on tissue and are employed in 



USES OF ELECTRICITY IN DENTAL THERAPEUTICS 785 

general therapeutics. The well-known Finsen light is so arranged 
as to produce a cold but highly chemic white light useful in superficial 
diseases. Aside from the use of a blue light as a possible means of 
inducing an analgesic condition for operative purposes (see page 526) ; 
or its application to painful swellings of the face (or joints if recom- 
mended by a physician) colored lights have little application. 

The heat of electric light globes of some size (100 candle power) 
is also employed by means of a parabolic reflector for the purpose 
of activating the blood and lymph circulation which is usually further 
stimulated by massage, dry cupping, etc. An .x-ray apparatus 
develops ultra violet light (yellowish green to the eye) by passage of 
an interrupted electric current through a Crooke's vacuum tube. 

The color of the light in the tube depends upon the degree of vacuum. 

The chemic quality of the light rays passing through tissue * % to a 
photographic plate or film gives it its value in diagnosis while its 
chemic effects are utilized in therapeutics, especially in superficial 
diseases as lupus and carcinoma. (See Radiography.) 

2. Mechanical vibration is applied to tissue by means of apparatus, 
delivering a rapid series of light blows as the applicator (ball, water- 
bag, etc.) is passed over the surface. The circulation and lymph 
flow is activated and stases of various degrees and consequences 
relieved. It is vibratory massage of tissue. 

Electricity is not an essential feature of vibratory massage and 
does not enter the tissues being massaged, but is a convenient source 
of power for a mechanical vibrator (see page 533). 

Electric Vibratory Massage. — A certain amount of contraction of 
muscular tissue (including those of bloodvessels) may be induced 
by the ordinary Faradic current which consists of unidirectional, low- 
voltage electricity frequently interrupted. With infrequent appli- 
cation or interruption a marked muscular contraction occurs which 
may be utilized to stimulate respiration as in poisoning or drowning 
cases, while with constant contact a cell and muscular agitation is pro- 
duced. The passage of the Faradic current has been experimentally 
shown to have beneficial effects on the general nutrition of normal 
experimental animals, they having gained weight faster than the 
control animals. 

As each dentist should possess a small Faradic apparatus for 
diagnostic purposes, it may be used with the positive pole (sponge 
electrode) passed over a swollen face, the negative in the hand. The 
current is controlled by the core cover (tube of Duchenne). The 
application should in this case be continuous and the characteristic 
tingling sensation is to be expected. This treatment is known as 
"Faradization." (See Fig. 477,) 
50 



786 USES OF ELECTRICITY IN DENTAL THERAPEUTICS 

Electric vibration or vibratory massage of cells is supposed to be 
effected by the so-called "violet ray" apparatus. 

This is the application of the alternating current which has been 
"stepped up" by special transforming devices until a very high 
degree of voltage (intensity of current) with very low amperage 
(quantity of current) is attained. The current no sooner flows in one 
direction than it flows back in the other, in both with varying intensity 
during the flows which is the characteristic of an alternating current 
and is called "oscillation." 

Fig. 728 




Rogers violet ray apparatus. 



The alternations (of direction) are so frequent per second that the 
current is properly called a "high frequency" current. In such high 
frequency muscular contraction is not noted as it is in lower alterna- 
tions (below 10,000 cycles). As it passes into vacuum tubes of varying 
shapes (electrodes) the ether therein is agitated and varying colors 
are produced according to the degree of vacuum present. In dental 
apparatus a violet color is developed, hence the term "violet ray." 

There is no need for two electrodes as the current passes in and 
back or may be transmitted via the body to another similar electrode 
actuating it also to violet color. Its conduction through the body 
may be assured by using a metal conductor (as a chair arm, etc.) 
on the opposite side. Glass (or the enamel of teeth) does not insulate 
it and even rubber will transmit it at points opposite the electrode; 
also it penetrates clothing and will jump a fair air space and actuate 
a similar electrode held near it even if the spark does not jump the 
space. In practice the high frequency current (alternating) may be 
developed from the commercial direct current by special transforming 



USES OF ELECTRICITY IN DENTAL THERAPEUTICS 787 

devices included in the commercial forms of apparatus, so that it 
is only necessary to attach to the ordinary light socket or switchboard 
(full voltage). A certain amount of ozone is produced about the 
electrode by the chemical change in the oxygen of the air as occurs 
about a Crookes's tube. The electrical agitation is supposed to effect 
great activity in the cells increasing metabolism (chemical change), 
also to stimulate circulation. It is used for this purpose in pyorrhea 
alveolaris. Possibly ozonization may play a part (see page 685). 

It is also an analgesic agent and has been employed to obtain 
access to parts (as third molar gums, abscesses, etc., when patients 
are unable to open the mouth. For this the use of the broad elec- 
trode for twenty minutes on the face over the part is recommended. 
Vaselin should first be applied. While its use in dentistry as a caustic 
is not known, in medicine a long, sharp spark from a single pointed 
special electrode (fulguration) has cauterant properties employed on 
small growths. It might be used in certain cases were not the electric 
cautery available. 

3-4. The introduction of drugs into tissue by means of a galvanic 
current has long been known. For purposes of definition a primary 
current from a battery and a commercial direct current (produced 
by a dynamo) are the same and understood as galvanic so far as 
therapeutics is concerned. It only remains to reduce the 110 volt 
direct current by means of a suitable resistance to about 30 or 40 
volts. From that point on a special resistance (current controller) 
is used either with the direct commercial current or direct, battery 
current. The. original cataphoric apparatus introduced by Gillette 
was actuated by a battery of from 20 to 30 dry cells, silver chlorid 
preferred, but Leclanche cells or others could be used. This developed 
the electricity which was taken from the positive pole (carbon) to 
the special resistance, thence to a milliamperemeter (recording the 
quantity of current passing in spite of the resistance of the patient, 
plus the special resistance), thence to the tooth cavity (in which a 
solution of cocain hydrochlorid was placed on cotton and under the 
positive electrode), thence via the pulp, patient's tissues, to the arm 
and hand to the negative electrode and back to the negative (zinc) 
pole of the battery thus establishing a direct current circuit. 

In its passage from positive to ■ negative certain substances as 
cocain are carried bodily with the current apparently intact (cata- 
phoresis). If the current carries an electronegative substance such 
as iodin intact from the negative toward the positive pole it is called 
anaphoresis. 

If the current decomposes a chemical compound into its constit- 
uent parts (or ions) the ions which are naturally electropositively 
charged travel to the negative pole (cations), while the other ions 



788 USES OF ELECTRICITY IN DENTAL THERAPEUTICS 

naturally electronegatively charged travel toward the positive pole 
(anions) . This is electrolysis (or electrolytic dissociation) and its use 
in therapeutics is termed electrolytic medication. The term ions refers 
to the electropositively charged or electronegatively charged particles 
in a molecule. They are set free by electrolysis and are the conductors 
of electricity. Thus in electrolysis of water H being positive conducts 
the positive current flow and is attracted to the negative pole (cation) 
while O being electronegative carries the negative current flow in the 
opposite direction to the positive pole (anion) . ' 

Custer 1 illustrates these opposite current flows by a stream of 
wagons crossing a bridge in one direction carrying one kind of mer- 
chandise while another stream crossing in the opposite direction carry 
merchandise of another kind. 

Sturridge 2 objects to the terms cataphoresis and anaphoresis as 
here defined, claiming that probably in all cases an ionic effect is 
produced. He does not say an electrolytic production of ions, but 
a carrying of cocain ions, for example, as a fraction of a molecule 
into the pulp tissue. He also says: "It is quite conceivable that 
a substance like cocain when acted upon by water is split up 
into ions and in this state is readily introduced, etc." Again 
he states that Leduc introduced strychnin into a rabbit's ear by 
passing a current with positive at the ear. The animal died in 
typical strychnin convulsions. 

He cites other cases of actual transference of substances into tissue 
as alarming cocain poisoning from application with the cataphoric 
current positive pole at tooth pulp. Considering the complex nature 
of cocain and strychnin and that electrolysis evidently did not occur 
otherwise the strychnin and cocain would have been dissociated . 
into their ions and could not have produced their characteristic effects, 
it seems rational to admit the term cataphoresis at least. As ana- 
phoresis occurs against the general current flow (from negative to 
positive) it must be defined as an anodic travel of negatively charged 
ions; that is, the chemically unbroken substance is an anion. 

In electrolysis the following elements of a molecule arrange them- 
selves into their respective electric group, becoming anions or cations 
as may be: 



Electropositive or Cations. 


Electronegative or Anions, 


Copper. 


Arsenic. 


Iron. 


Bromine. 


Hydrogen. 


Chlorine. 


Mercury. 


Iodin. 


Potassium. 


Nitrogen. 


Sodium. 


Oxygen. 


Zinc. 


Sulphur. 


All basic radicals. 


All acid radicals. 


1 Dental Electricity. 


2 Dental Electo Therapeutic: 



USES OF ELECTRICITY IN DENTAL THERAPEUTICS 789 

In order to obtain penetration of the cations from their salts in 
solution the positive pole must be applied to the point from which 
they are to be driven and the negative pole on the side they are to be 
delivered ; for example, to reach apical tissue, the tooth root and the 
hand respectively. For the anions the poles are reversed. 

The ions available for such therapeutic purposes as sedation, 
stimulation, disinfection and counter-irritation are ably suggested 
by Sturridge, Prinz and others. 

Zinc ions may be developed and driven in by the use of a 3 to 5 
per cent, zinc chlorid aqueous solution, a positive zinc, platinum or 
steel electrode and 2 to 3 m.a. of current, the negative being at the 
hand, etc. It is considered antiseptic and useful in apical suppuration 
or pyorrhea. 

Copper ions may be dissociated by the use of 3 per cent, aqueous 
copper sulphate solution, a positive copper electrode and 1 or 2 m. a. 
Negative pole at the hand. A copper spatula may be used in the 
gingival trough and a copper probe in a fistula in like manner. 

Silver ions are obtained by the use of weak aqueous silver nitrate 
and a positive silver electrode. Iodin ions, a weak aqueous solution 
of the tincture of iodin is used with a negative platinum electrode, 
positive at the hand as it is electronegative. It is used for disinfecting 
and healing apical tissues or to be driven into the gum surface over 
the apex in case of apical pericementitis. Chlorine ions are developed 
in like manner from 1 per cent, aqueous sodium chlorid solution, if 
penetration of apical tissue is desired. Prinz 1 suggests the positive 
in the canal for canal sterilization, using a constant (30) as a means 
of calculation of the time of application required according to the 
formula : 

30 

— -. — v = Time (for example here 10 minutes). 

m. a. (for example 3 m. a.) 

Oxygen ions may be obtained from the loosely held of H 2 2 by 
the use of a negative platinum electrode in the tooth, positive at the 
hand. The ordinary use of H 2 2 is with the positive at tooth (cata- 
phoresis) but occasionally the reversal of the poles is valuable in 
bleaching (see page 507). 

The salicylic ion is dissociated from salicylate of soda solution on 
cotton by a broad positive electrode (1§ inch square) placed over 
site of neuralgia and a 5 inch square negative electrode over upper 
cervical vertebrae. (Sturridge.) 

Sturridge also commends a solution of argyrol as sedative and 

1 Dental Cosmos, April, 1917. 



790 USES OF ELECTRICITY W DENTAL THERAPEUTICS 

healing in acute gingivitis or sloughing gum, positive platinum or 
silver electrode at gums, with doubt as to ionic effects. 

The cocain ion has been considered under cataphoresis. 

The advantages of electrolytic medication are the production of 
nascent ions and their introduction into the tissues as against mere 
superficial contact. 

Technic. — With the exception of application external to the tooth 
as in pyorrhea the rubber dam is to be adjusted for insulation in 
dentin and pulp work and for asepsis in canal work. Any external 
asepsis needed is to have attention. In either cocain cataphoresis or 
canal work amperage is important and is governed by the sensation 
of the patient. 

In case of commercial current a "grounding" of the circuit is to be 
avoided by the use of a rubber mat under the chair and avoidance of 
metal parts of the chair or cuspidor by the patient. Metal rings, etc., 
are to be removed to prevent blistering. The apparatus is set with the 
volt selector (rheostat or resistance) at zero, the wrist pad or metal 
electrode of ample dimensions to prevent a blister is moistened with 
salt solution and adjusted to or in the left hand, the proper pole being 
observed. The medicament being used is applied and a proper 
electrode applied to the tooth. The current is now slowly turned in 
and as pain is felt the indicator of the current controller is turned 
back a little then advanced again until full toleration is obtained. 
In the case of cocain anesthesia the lack of response to a slight 
jump of the current indicates pulp anesthesia and one may operate 
at least on the dentin. The milliamperemeter will indicate the 
amount of current flowing against the resistance. This is only of 
value as showing that electricity is passing (and for scientific statistics) 
in cocain cataphoresis, as toleration is the essential point. The instru- 
ment may even be dispensed with. It has value in root sterilization, 
however. (For details of this see page 496.) When through, the 
indicator of the controller is gradually turned back to zero, thus 
turning in the resistance; the electrodes are then removed. 

The high frequency current has also been suggested as a cata- 
phoric agent in hypersensitive dentin. A pointed electrode and a 
very mild current is used against a crystal of carbolic acid placed in 
the cavity for from a half-minute to a minute or if still sensitive a 
half minute longer (Hubbel 1 ) . Placing a crystal of novocain in the 
cavity, dipping the electrode in adrenalin solution and applying 
with a very mild current is also recommended by Hubbel for hyper- 
sensitive dentin and to get an exposure of the pulp. 

1 Quoted by Eberhart: High Frequency Manual. 



uses of Electricity in dental therapeutics 791 

He also uses it as a cataphoric agent for driving bleaching solutions 
in bleaching teeth, the apical region to be previously filled. 
Its value in sterilizing root canals is yet indeterminate. 

5. While not an anesthetic agent in itself a mild induced inter- 
rupted current has been used as a means of substituting a steady 
impulse or sensation along the nerve trunk which confuses the center 
of pain perception. The method at least in its refinement was intro- 
duced by J. Foster Flagg who used what he termed a Dental Helix. 
There was but one coil conveying the primary current which was 
interrupted in its course. The current was strengthened by an induc- 
tion core consisting of a bundle of wires. This was covered by 
a tube of Duchenne which could be drawn off the core. A water 
rheostat was used to reduce the current to the most delicate possible. 
The positive electrode was bayonet-shaped and of strong wire covered 
by hard rubber. A cup applicator at the end held a bit of wet sponge 
to be pressed against the gum above the tooth. The negative elec- 
trode was the metal casing of the handle of the same electrode and 
made the contact with the hands. The current therefore passed 
through the gum to the arm and hand holding the applicator. This 
instrument was satisfactory in some cases, the chief difficulty lying 
in the fact that it was apt to slip causing a shock or be in the way. 
It may be that a modified applicator may render it of more utility. . 
In extraction the positive pole of the helix was attached to the forceps 
by special cords, the negative placed in the hands and was said to 
give some satisfaction. 

6. Any mild interrupted current capable of increase or a mild 
high frequency current may be used as a means of diagnosis of pulp 
vitality.. A small Faradic battery energized by a single dry cell is 
sufficient for a current too strong for application. A rheostat elec- 
trode is described on page 486 by means of which a very delicate 
current may be obtained so that if desired a filling may be touched. 
Ordinarily the platinum point is wound with cotton wet with normal 
salt solution and the enamel of each tooth suspected touched. The 
strength of current is first determined by trial on a sound tooth. 
Either pole may be used, the other being in the hand. A positive 
response indicates vitality, but no response to a strong current does 
not of necessity indicate death. Even a filling or the bare dentin 
may occasionally fail to conduct so as to produce response while 
on drilling sensitivity may be obtained, but taken altogether it is a 
satisfactory means of testing, especially if taken along with other 
tests or indications. The details and comparison with other tests 
are given on page 483. 

The high frequency current is of value, also as an electrical test 



792 USES OF ELECTRICITY IN DENTAL THERAPEUTICS 

when applied to the enamel, though even with this remarkable differ- 
ences of response in apparently normal teeth appear. In posterior 
teeth the sparks tend to jump to the cheek rendering it necessary to 
use great care. One should always use mild applications at first. 

7. As a sterilizing agent electricity has been written of both as 
an efficient agent and as failing in that respect. Usually it is employed 
as previously described as a cataphoric, anaphoric or electrolytic 
force. As an aid in bleaching it has been employed as described on 
pages 507 and 789. 



CHAPTER XXX. 
ASEPSIS AND STERILIZATION. 

Sepsis signifies a condition in which bacteria are present and while 
some are harmless, others are liable to cause infective conditions. 
Asepsis signifies the condition of absence of bacteria. The close 
application of these definitions refers to the part being operated upon 
and anything coming into contact or relation sufficiently close to 
cause direct infection. 

The saliva, all cavities of decay, gingival margins, and root canals 
containing dead pulp; all used instruments and those lying in the 
cabinet, the air, unsterilized hands, the chip syringe, medicine bottles, 
etc., are all septic in principle. The two aseptic areas are the root 
canal containing a freshly exposed vital pulp and tissue beneath the 
healthy mucosa. There is but one general method of attaining asepsis 
and that is through antisepsis. This involves absolute mechanical 
cleansing and the employment of germicidal substances or heat 
to destroy any remaining bacteria. Ideally, even the office air should 
be filtered, the office washed down, all persons disinfected, the parts, 
the hands and the instruments, etc., sterilized. 

To attain all this is at present obviously impossible. Even in sur- 
gical clinics it is impossible and even in private surgery of aseptic 
surgeons inconsistency obtains. All that is possible is reasonable 
asepsis, but this must be insisted upon. Fortunately the air contains 
but few if any pathogenic bacteria, those principally feared being 
found in the mouth and on the hands and instruments. The general 
surgeon also guards against infection from the hair which in dental 
work is probably less necessary, except in more urgent cases as 
apicoectomy or root work. The dentist has also an advantage in 
that powerful germicides may be employed before, during the con- 
tinuance of his work or directly thereafter. 

The details of attaining asepsis, relate to the operator, the appa- 
ratus and instruments employed and the field of operation and 
each will be dealt with separately. In all cases it must be noted that 
sterilization to attain asepsis has nothing to do with the inhibitive 
action of antiseptics employed to gradually lessen the number of 
bacteria or restrain their action while the tissues destroy bacteria 
by phagocytic action. This latter is a principle of therapeutics, not 
a surgical disinfection. Occasionally as where caustics are used both 

bacteria and tissue are destroyed (see Aphthae). 

(793) 



794 



ASEPSIS AND STERILIZATION 



The Operator. — Extreme personal cleanliness upon the part of an 
operator is clearly the first step in asepsis. The best class of dentists 
are exceedingly neat as regards personal habits; daily bathing, care of 
the nails and of the skin, and immaculate linen form as much a part 
of the day's labor as dental operations per se. The virtues of soap 
and water, wherever they may be applied, are regarded as a very 
important item in preventing infection, but ordinarily used clothing 
is always unsafe. A surgeon usually makes a complete change to 
sterile clothing, gowns and headgear. 

Personal sterilization in dentistry relates to the hands, particularly 
to the finger-nails. The space under the nails is a favorable habitat 
for many organisms. 

Fig. 729 




Ik 



Castle steam sterilizer. 



Xails kept short and smooth may be more readily cleansed than if 
long and ill-kept, and should be cut so that they nowhere project 
beyond the tips of the fingers. Their mechanical cleansing should 
be done with smooth instruments, not sharp knife-blades; the latter 
produce rough surfaces, which furnish spaces for lodgement of bacteria. 
There is but one effective method of washing beneath the nails; it is 
that followed by the general surgeon. After dipping the soap in water 
as hot as can be borne by the hands, all of the finger-nails should be 
made to scrape the soap until the spaces under the nails are filled 



THE OPERATOR 



795 



with it. After this coarse hand-brushes are used to scour every 
part of the hands with soap and water as hot as can be borne. Special 
nail-brushes are next used to scrub beneath the nails, driving out 
piecemeal the soap masses there. The general surgeon continues the 



Fig. 730 



Fig. 731 




*> 



* 




Streptococcus viridans from tooth socket 
after extraction from very small infected apical 
area. Cause of arthritis and general nervous 
breakdown. (Callahan. 1 ) 



Staphylococci from finger tips after washing. 
(Callahan. 1 ) 



Fig. 732 



Fig. 733 





Infection from paper point transferred from the 
box (opened for some time.) (Callahan. 1 ) 



Infection from cotton twisted with ordinarily 
cleansed fingers. (Callahan. 1 ) 



Dental Cosmos, January, 1918. 



796 ASEPSIS AND STERILIZATION 

scrubbing until the nails are scrupulously clean. Ten minutes is 
the usual period. The soap usually used is Castile, or soap made 
from palm oil, etc., but antiseptic soaps, such as ethereal soaps, may 
be substituted with advantage. Tincture of green soap is fairly 
effective (see below). To avoid touching with the hands washstands 
are arranged with foot operated faucets. 

Sterilization of the cleansed hands is insured ; (1) by immersing them 
in germicidal solutions, such as biniodide of mercury, 1 part; methyl 
alcohol, 500 parts for two minutes and then washing off in a 1 to 
3000 solution of the biniodide (Lockwood) ; (2) in a saturated solution 
of potassium permanganate, then in saturated solution of oxalic acid, 
both warmed, then in warm water; (3) rubbing the hands with a paste 
of mustard flour and water for three minutes and washing off with 
sterilized water is effective (Nancrede); (4) iodin trichlorid, 1 per 
cent, having been shown to be germicidal in fifteen seconds by Waas, 
may be used for one minute. It is very convenient, keeps indefinitely 
and does not discolor the hands. 

It may be poured over the wet hands and rubbed in or the hands 
dipped in a vessel containing it. If the patient dismissed has possessed 
an unusually septic mouth, or has been a syphilitic, for example, the 
time for hand cleansing and sterilization is to be prolonged; if syphi- 
litic, every instrument used is transferred to separate vessels contain- 
ing antiseptic solutions or boiled, and the hands are viewed as highly 
infected. Chancres have from time to time appeared upon the 
fingers of dentists as well as physicians. In a known syphilitic case 
one might use the rubber gloves worn by surgeons; at any rate all 
abrasions should be covered with collodion. 

Sterilization of Apparatus. — The office in general should be kept 
scrupulously clean. Boiling of linen during the washing process is 
sufficient. For continued antisepsis of towels for surgical purposes, 
a dust-tight cabinet in which formaldehyde vapor is liberated from 
an open dish, containing the 37 per cent, solution may be used con- 
tinuously. The latter furnishes the necessary moisture. Aseptic 
napkins are a problem. It is said all contain bacteria in spite of auto- 
claving at the factory. The above formaldehyde cabinet for routine 
work and special autoclaving for more than ordinary operations 
seems safe enough from the clinical viewpoint especially as these 
are air bacteria. Muslin strips or the above cheesecloth napkins 
cut into strips may be considered in the same light. Each is thrown 
away after use. 

Head rest covers are a source of head infection transmission and 
bracket table covers are a medium of transference and should be 
changed after each patient, as should a cotton catcher, if one is used, 
as this so-called sanitary object is questionable even on the same 



STERILIZATION OF APPARATUS 



797 



patient and a certain medium on two. If of paper it should be thrown 
away, if of other substance, sterilized. 

If a hydraulic saliva ejector be used, the glass mouth tubes should 
be changed for each person, a sterilized tube being substituted 
directly before its use is required and not used after being hung up. 
A number of these tubes should be in use, and may be sterilized after 
washing by placing them in a formaldehyd solution for a few hours. 
Tumblers and mouth mirrors may be sterilized in like manner. 
The cloudiness of saliva tubes is produced by the formation of sali- 
vary calculus, and may be removed by the use of acidulated water. 1 

At the close of each day a large cup should be filled with an anti- 
septic solution, which is to be drawn through the tubing of the ejector 
to keep it in a reasonably aseptic condition. The flow being from 
the patient, this is not a probable source of infection. 

Rubber dam may be sterilized by boiling water, but it is more 
safe and cleanly to use a new piece for each patient. It should be 
washed and then dusted with borated talcum powder. 

The water used for douching cavities should be boiled previous to 
placing in the warmer, and should have a little pleasant antiseptic 
added to it. The rubber bulb or handled part of water syringes, 
chip syringes, etc., are rarely sterilized, but are a ready source of 
hand infection and transference. The logical method is to have a 
number and to wash and throw the used one into a formaldehyd 
solution after using. The point should be kept out of infective areas, 
saliva, etc., but if infected may be passed through the gas flame 
before returning to the patient. 

Sterilization of Instruments. — Nancrede 2 states that all pyogenic 
cocci, and even anthrax spores, are killed by boiling instruments for 
two minutes in a 1 per cent, solution of sodium carbonate, which also 
prevents rusting. For hand pieces, etc., boiling in almond oil is 
suggested by Goadby. Pond 3 after experimentation claims the fol- 
lowing minimum exposure to various sterilizing agents to be necessary. 



Subjected to 


Boiling 

water. 


Superheated Steam and 
steam. hot air. 


Steam in 
autoclave. 


Hot air at 
180°. 


Dipped iFormalde- 

in molten hyde in a 

metal, j cabinet. 


Instruments 














Burs assorted . 


25 min. 


1 to 2 min. 


15 min. 


25 min. 


1£ hours 20 sec. 3 hours 


Broaches assorted 


20 min. 


1 min. 


10 min. 


20 min. 


1 \ hours 


2 hours 


Cotton on 














broaches . 




3 min. 


20 min. 




.... 10 sec. 




Absorbent paper 
















points 




50 sec. 


20 min. 






10 sec. 




Gutta-percha 
















points 






15 min. 











1 Thornton: Dental Review, 1903. 2 Park's Surgery by American Authors. 

3 Jour, of Nat. Dental Assn., April., 1919, p. 360, 



798 



ASEPSIS AND STERILIZATION 



Zametkin 1 has suggested for chemical sterilization three Mason 
jars: (1) Containing pure lysol in which the instruments remain 
several hours. (2) Containing alcohol to wash off lysol. (3) Con- 
taining alcohol to further wash off lysol. He recommends igniting 
the adherent alcohol. 

Mouth mirrors and other instruments which can be wet may be 
placed for one-half hour or longer in a covered jar containing 20 per 
cent, formaldehyd, to which borax has been added to saturation. 
Rusting is prevented by borax (Williams). Even hand pieces acci- 
dentally placed in this solution have been found uninjured after 
hours of immersion, but must be wiped off and liberally oiled. If 
allowed to stand they rust badly. 

Fig. 734 




The Flaherty molten metal sterilizer. 



Broaches require special care. According to Pond (see above), 
the best method is to dip them or the cotton on them into molten 
fusible metal at 150° C. or more for ten or fifteen seconds (Fig. 734). 
Even new broaches should be sterilized. They are then placed in a 
dish containing^, germicide. Still another method is to previously 

1 Dental Digest, December, 1914. 






STERILIZING THE FIELD OF OPERATION 799 

wrap the broaches with sterile cotton with the sterile fingers and auto- 
clave (Miller). This may be supplemented by placing in a formal- 
dehyde container for at least ten hours (D. Guilford) (see page 
800). Gutta-percha points are kept in 70 per cent, alcohol or 
a bottle containing dichloramine T. on cotton attached to the 
cork or 10 per. cent, formaldehyd solution. They can be removed 
and placed between the folds of a sterile napkin until required. 
Wire bur cleansers should be wet with 70 per cent, alcohol while 
burs are being cleansed. Absorbent cotton may be sterilized by steam 
in a Castle sterilizer for twenty minutes and kept in small envelopes. 
The corner is torn off when to be used (Black), or a wide-mouthed 
bottle may have a tablet of paraformaldehyd with the cotton or 
Prinz's method above. 

Broaches, trephines, and other small points requiring to be kept 
sterile may be placed in a bottle such as are sold containing gold 
cylinders, and kept wet with any essential oil or carbolic acid. 

G. Zederbaum 1 suggests sticking the shanks in the cork of a wide- 
mouthed bottle containing a non-rusting germicide; when to be used 
the cork is to be transferred to another bottle of like size containing 
alcohol and shaken to remove the antiseptic. They may then be 
washed in sterilized water. 

Extracting forceps require careful mechanical cleansing and pro- 
longed boiling after each use, for perhaps more cases of infection, 
and of many kinds, have resulted from unclean forceps than from 
all other causes combined. 

Instruments, such as hand-pieces, electric mouth mirrors, etc., 
which cannot be conveniently soaked may be wiped off with 70 per 
cent, alcohol in which the writer places a small quantity of a mix- 
ture of oil of gaultheria and cassia and then subjected while wet 
with this for one hour to formaldehyd gas. Any closed vessel may 
have cotton rolls saturated with liquid formaldehyd placed therein. 
Enough gas is given off to disinfect. Lacking a special apparatus an 
aluminum omelet pan with the handle filed off makes a convenient 
and not unsightly sterilizer. If desired, all the instruments may be 
so sterilized. These methods involve the employment of several 
instruments of each kind, an economy of time in any event. The 
entire instrument case may be disinfected by placing a formalin 
tablet in each drawer (Miller). The instruments used in conductive 
anesthesia are kept in alcohol 2 parts, glycerin 1 part, and the 
platinum needle flamed as used. 

Sterilizing the Field of Operation. — The mouth in general is difficult 
of immediate sterilization but a brushing with a cheap personal 
brush followed by a forcible spray of hydrogen dioxid to remove 

i Dental Cosmos, 1907. 



800 ASEPSIS AND STERILIZATION 

loose material and this followed by a germicide as below upon a 
selected area renders it as sterile as can be expected for ordinary 
cleansings or extractions, etc. The peroxid wash on page 615 is germi- 
cidal. While working on pyorrhea pockets this may be previously 
injected or the instrument constantly dipped in a small quantity of 
Talbot's iodin placed in a medicament glass or in this instance the 7 
per cent, official tincture may be used for the instruments. If deep 
operation is intended as in root amputation, hypodermic injections, 
etc., the mucosa should be gently scrubbed with Talbot's iodo- 
glycerol one-fourth strength or tincture of iodin (tincture 7 per cent., 
5 parts, ethyl alcohol 3 parts, making a 4 per cent, solution) or 1 per 
cent, trichlorid of iodin (see page 796). The peculiar "running or 
diffusible character of iodin renders it of value in penetrating 
reasonably inaccessible parts. While iodin is said to be soluble only 
in 5000 parts of water, the tincture seems readily diffusible in water 
in almost all proportions. Hare describes it as in general use in 
surgical operation for skin disinfection in the above 4 per cent, solu- 
tion and for delicate tissue may be removed with alcohol. Washing 
the skin or mucosa is undesirable as the epithelial cells will swell and 
not be penetrated. 

Iodoglycerol in 25 per cent, solution has been repeatedly tested 
by Drs. Tuttle and Saxon, of Philadelphia, and the parts so treated 
found sterile. This exceeds 4 per cent, of iodin and is also not irri- 
tating. Prinz suggests iodine 2 parts, acetone 4 parts (see page 776). 

The method is so simple and rapid that other less valuable and 
laborious ones may be set aside. 

When the operation is serious, the face and head of the patient 
should be covered with a sterile cloth mask with apertures for the 
eyes and mouth or towels covering all but the parts to be left exposed. 
Such parts of the face as are exposed may be wiped with 1 per cent, 
iodin trichlorid or other germicide. 

In handling roots which have been properly sealed at the apex, 
but which require disinfection, owing to infection in handling, 
tincture of iodin or trichlorid of iodin 1 per cent, should be applied 
and dried out just before setting a permanent or temporary crown. 

In the maintainance of asepsis in root canals after disinfection or 
to attain it, saliva must be excluded. Ordinarily the rubber dam is 
applied, tincture of iodin used and then washed off with 70 per cent, 
alcohol, before any work on canals is done. As an alternate, phenol 
followed by alcohol is recommended by Lee. The details of this and 
further canal disinfection are described on page 448, etc. In root 
canal work when asepsis is attained it should be maintained during 
root filling by attention tQ every detail of asepsis; even the bottles 



STERILIZING THE FIELD OF OPERATION 



801 



should not be handled. One per cent, iodin trichlorid or bichlorid 
of mercury in H 2 2 , 1 to 500 should be used on the fingers when 
suspected. Chloroform is said to be germicidal in one minute and to 
an extent may be considered in the act of root filling. 



Fig. 735 




Blue Island spraying and nebulizing outfit No. 3. Especially designed for the 
orthodontic patient's home use, to keep appliance clean and mouth in hygienic con- 
dition. Also for home treatment of pyorrhea alveolaris. 1, atomizer for spraying 
oil or water; 2, automatic cut-off; 3, Nozzle for direct spray; 4, universal nozzle 
(throws spray up, down, right or left, or at any angle in the vertical plane) ; 5, nebulizer; 
G, powder-blower; 7, oxidized metal rack; 8, air pressure gauge; 9, black rubber tubing 
conducting air from tank; 10, black rubber tubing conducting air from pump to tank; 
11, air compressing pump; 12, air tank (capacity, 400 cubic inches). 



Cavities of decay are a problem, but strong phenol followed after 
a few minutes by alcohol or the Howe silver nitrate treatment (as on 
page 477) or the use of persistent antiseptics in the cement used 
(as thymol, see page 341) are practical. 

. For very thorough mouth disinfection thoroughly cleanse the teeth 
and use the antiseptic between them upon floss silk. For surgical 
work or etherization very active work should be done. Wadsworth, 1 
in an investigation of mouth washes and their action on pneumo- 



1 Dental Cosmos. 



51 



802 ASEPSIS AND STERILIZATION 

cocci, found but little value in the ordinary wash or even solutions 
of formalin, lysol, or H2O2. He found that 

3— Alcohol ; 30 parts 

Water 70 parts 

Glycerin and salt, a small quantity added. 

was very effective in destroying the bacteria. 

Waas found iodin trichloride 1 to 1000 in water, to be germicidal in 
three minutes. 

The routine practice of scaling and polishing the teeth and pre- 
scribing an antiseptic mouth wash prior to the commencement of a 
series of sittings is to be highly commended. 

In scaling the writer uses antiseptic washes freely during the entire 
operation and tincture of iodin, etc., on the instruments (see pages 799, 
800). 

If ulcerations or inflammatory conditions exist, or if a suspicion 
of syphilis exist, the sterilization is to be prolonged. 

A deep infection may usually be prevented during the treatment 
of pyorrhea alveolaris and pulp gangrene by attention to the ster- 
ilization of the infected tract before beginning work upon the parts 
or during its progress. These methods have been indicated in the 
discussion of these subjects. 

In orthodontia the patient may use an antiseptic spray actuated 
by a small air compressor. This is also useful in the course of pyorrhea. 

The operator should select a method and consistently pursue it. 



INDEX 



A 



Abnormal food supply, 18 

nerve supply, 18 

physical conditions, 18 

waste removal, 18 
Abrasion, 199 

acids in, 207 

in animals, 208 

of calculus, 205 

degrees of, 201 

during sleep, 201, 213 

effects of, 209 

from clasp, 207 

gritty powders as cause of, 207 

labial and approximal, 203, 207 

lingual, 203, 205 

occlusal, 200 

pulp hyperemia in, 210 

relation to caries in, 209 

tooth-brush in, 203, 206 

treatment of, 210 
Abscess, apical, acute, 512 

after treatment of, 534 
causes of, 514 
clinical history of, 520 
diagnosis of, 523 
extraction in, 529 
guards in, 527 
necrosis from, 530 
on opening teeth, 504 
pathology of, 515 
radiography in, 538 
scar threatened in, 533 
stages of pus formation in, 

516 
symptoms of, 515 
systematic stopping in, 

540 
systemic complication in, 
519, 522, 529, 530, 532, 
534, 554. (See Infec- 
tion.) 
treatment of, 525 
chronic, 520, 535 
blind, 555 

discharging via canal, 535 
grades of, 535 
necrosis from, 563 
not healing, 548 
radiography in, 538 
scar from, 554 



Abscess, apical, chronic, symptoms of, 
538 
systemic complications in, 

557. (See Infection.) 
in temporary teeth, 566 
treatment of, 539, 545 
varieties of, 535 
with fistula, 541, 544 
around third molar, 109 
perforation of bone in, 528 
pericemental, 698 
pointing in, 43, 518 
of pulp, 410 
syringe, 546 
Absence of teeth, 192 
Absorbent organ, 91 
Acacia, use of, 78 
Accidents to teeth, 599 
Acetanilid as cause of hemorrhage, 30 

use of, 405, 532 
Acid, extraneous effect of, 220 

fruits, use and effects of, 87, 220, 336 
neutralization of, 223, 262, 284, 336, 
344, 455, 757, 759 
Acidosis, 622 

Aconite, tincture of, 109, 391, 527, 572 
Aconitin, use of, 109 
Actinomycosis of mouth, 734 
Adenoids in mouth breathing, 97, 102 
Adrenalin, use of, 326, 430, 503 
Age as predisposition, 267 
Agenesia of enamel, 166 
Air, compressed, use of, 323, 504, 800 

use of, 323, 548 
Alcohol, injection of, 718 

use of, 77, 131, 323, 332, 344, 391, 
396, 467, 532, 613, 629, 800 
Alcresta ipecac, use of, 689 
Alimentary canal infection, 745. (See 

Dentition.) 
Almond, bitter oil of, use of, 336 
Aloin compound, use of, 624 
Alopecia from dental disease, 716 
Alum, use of, 31, 77, 396, 405, 420, 476, 

477, 482 
Alveolar process, fracture of, 600 
Alveolitis, postextraction, 601 
Amalgam, copper, use of, 351 

facing, 442 
Ameba of pyorrhea, 653 
Ameloblasts, 141 
Ammonia, use of, 334, 344, 431 
(803) 



804 



INDEX 



Ammonium bifluorid, use of, 682 
Ammonol, use of, 314 
Amputation of roots, 771, 776 
Amyl nitrite, use of, 433 
Analgesia, 312, 526 
Anaphoresis, 496 
Anemia, 22, 24, 33, 268, 549 
Anesthesia of apical tissue, 314, etc. 

cataphoric, 328 

conductive, 314, 404, 428 

diplceic, 112, 322 

by electric current, 791 

general, use of, 312, 428 

infiltration, 321 

mucous, 321 

of nerve trunk, 428 

pressure, 429, 431 

of pulp, 429 

reflex, 322 
Angina, Ludwig's, 110, 739 

simplex, 739 

Vincent's, 608, 615, 740 
Angle, classification of malocclusion by, 

98 
Anise, oil of, use of, 336 
Ankylosis, dental, 579 
Anomalies of teeth. See Malformations . 
Antacids. See Acid Neutralization.) 
Antikamnia, use of, 314 
Antipyrin, use of, 717 
Antiseptic powders, antiseptic washes 

and, use of, 78, 613, 755, 801 
Antiseptics, use of, 78 
Antitoxin streptococcus, use of, 1 12, 532 
Antrum, empyema of, 542, 550, 717 
Aphasia from pulp disease, 403 
Aphthae, 724 

Apicoectomv, 475, 549, 550, 554, 556, 
578 * 

chapter on, 771 
Aqua regia, use of, 465 
Aristol, use of, 344, 349, 350, 467, 469, 

478 
Arsenic, accidents with, 443 

action of, on gum tissue, 443 
on pulp tissue, 435 
variations in, 437 

apical hyperemia from, 435-437 

formulas for, 439 

iodide of, use of, 400 

mummifying paste and, 445 

necrosis from, 444 

objections to, 438 

pentoxid, use of, 440 

pocket for, 443 

preparations, use of, 616 

pulp hyperemia from, 435 

in pulp nodule, 375, 376 

resistance to, 375, 437, 440 

seals for, 441 

suffusion from, 438 

use of, 335, 400, 405, 410, 435 
danger of, 443 
Arsenical fiber, 404, 430, 441 



1 Asepsis, 315, 448, 503, 793 

test for, 503 
! Aspirin, use of, 405 
Astringents, use of, 30, 78, 609 
Atomizer, use of, 804 
Atrophy, 33, 60, 159 

marginal, of gum, 625 

Harlan's method in, 626 
Atropin, use of, 574 
Attachment of teeth, 172, 175, 602 
Auto-intoxication, general malnutrition 
as cause of, 618, 745 
oral, effects of, 619 

B 

Bacteeia of blind abscess or granuloma, 
555 

in blood. See Septicemia. 

as cause of inflammation, 30, 41-47, 
398, 415 

chromogenic, 237 

conditions antagonizing, 18 

culture test, 540 

of dental caries. See Caries. 

increased virulence in, 504 

life of, conditions of, 18 

penetration of root tubules by, 567 
of secondary dentin by, 368 

plaques of, 244, 273 

of putrefaction of pulp, 488 

pyogenic, 42, 512, 513 

spreading of, in tissue, 519 
Balsam of Peru, use of, 682, 704 

of Tolu, use of, 131 
Band, dental, Fig. 118 
Bandage, use of, 30 
Baths, use of, 625 
Belladonna, use of, 214 
Benzoic acid, use of, 615 
Benzoin, use of, 131, 396, 404 
Bier's hyperemia, use of, 626, 685 
Bilein, use of, 625 
Biliousness, 745 
Bismuth preparations, use of, 79, 467, 

684 
Black, glands of, 556 
Black's 1-2-3 mixture, use of, 683 

operation for scar, 554 
Bleaching agents, use of, 238, 239, 506 
Blindness, dental cause of, 580 
Blood, alterations in, 21 

bacteria in. See Septicemia. 

coagulation of, 24 

extravasation of, 28, 38 

stasis of, 38 
Blue light, use of, 526 
Bodkin, wire, use of, 754 
Bone, caries of, 51, 544 

of face, embryology of, 133 

infection of, from dental lesions, 563 

inflammation of, 48 

of jaw, development of, 56 

necrosis of ? 50 



INDEX 



805 



Bone, necrosis of, from alveolodental 
a,scess, 553, 563 
from syphilis, 554 

perforation of, in abscess, 528 

regeneration of, 56 

resorption of, 50, 587, 590, 623 
in gingivitis, 623 
Borax. See Sodium biborate. 
Boric acid, use of, 570, 614, 717 
Boroglycerin, use of, 613 
Brandy, use of, 77 
Bridge work, use of, 589, 592 
Broaches, Downie-Kerr, use of, 452, 500 

Swiss, 460 

use of, 452, 460 
Bromides, use of, 313 
Bromural, use of, 313, 405, 528 
Brownin, 156 

Brush, use of, 203, 628, 751, 754 
Bruxomania, 201 



Caffein, use of, 532 
Cajuput oil, use of, 500 
Calcareous infiltration, 62, 377 
Calcific degeneration of pulp, 377 
Calcification of teeth, 141 

tubular; 360 
Calcium chloride, use of, 31 
lactate, use of, 31 
salts in blood, 633 
in pus, 647 
Calcoglobulin, 365, 371, 383 
Calcospherites in dentin, 141 
in enamel, 141 
in pulp nodule, 371 
Calculi, basis of, 62, 629 
Calculus, analysis of, 630 
hematogenic, 647 
origin of, 629, 632 
pyogenic, 628, 647 
salivary, 628 

analysis of, 630 
Black's experiments on, 632 
foreign bodies in, 630 
hardening of, 633 
hematogenic, 628 
mode of deposit of, 633, 649 
occurrence of, 636 
organic factor of, 632 
pathological effects of, 636 
pyogenic, 544, 556, 628 
removal of, 638 
scalers for, 639 
structure of, 630, 632 
treatment of, 638 
varieties of, 629 
sanguinary, 628, 647 
serumal, 628 
subgingival, 628, 644 
Calendula, use of, 615 
Callahan methods, 448, 452, 469 



Callahan's resin, use of, 455, 469 
Calomel, use of, 223, 624, 723, 730 
Campho-phenique. See Phenol camphor. 
Canada balsam, use of, 344 
Canals, accidents in opening, 464 
continuity of, lost, 464 
fining of, 466, 479, 534 

possibility of, 467, 475 
fillings, removal of, 500 
imperfectly filled, results of, 475 
inoperable apices, 475 
pastes in, 476 
root, enlargement of, 448, 452 

topography of, 452, 456 
in temporary teeth, 479 
Cancrum oris, 725 
Cantharides, use of, 447 
Cantilever wire spur, use of, 611 
Capping for pulp, 348 
Capsicum and myrrh, use of, 106 

plaster, use of, 528 
Carbohydrates in dental caries, 253, 255 
Carbolic acid, use of, 78, 110, 131, 420, 

433, 446, 528, 548, 572, 683 
Carbon dioxid, defective elimination of, 
217 
paper, use of, 594 
Caries of bone, 48, 544 
dental, 241 

acid medicines in, 262 

milk in, 255 
acids in, 247, 248, 255, 262, 269 
neutralization of, 259, 264 
age in, 267 
alkalies in, 255 
anemia and, 268 
arrangement of teeth in, 260 
backward, 278, 286, 296, 298 
bacteria of, 248, 249, 250, 253, 

287, 288 
bacterial plaque in, 244, 245, 

253, 269, 274 
bodily condition in, 268 
bottle feeding in, 266 
calcareous waters in, 262, 267 
carbohydrate fermentation in, 

253 
causes of, exciting, 241 

predisposing, local, 258 
systemic, 265, 277 
cavity production in, 284 
in cementum, 259, 293, 298 
chemical reactions in, 254, 284 
clinical history of, 294 
color of teeth in, 261 
debility in, 268 
deep-seated, 337, 339 
defects of fillings in, 260 
dentin in, 280 

decalcification of, 280 
destruction of, 283, 284 
secondary, 297 
diabetes and, 268, 269, 270 
diagnosis of, 301 



806 



INDEX 



Caries, dental, diet in, 253 
dyspepsia in, 268 
eburnation in, 292 
electrical theory of, 242 
in enamel, 273 

experiments in, 245, 262, 266 
- ferments in, 245 

filth as a protection from, 271 
foodstuffs in, 244, 245, 253, 255 
form in, 258, 273, 275 
general theory of, 244, 257 
glucose and, 254, 270 
glycogen in, 265, 268, 269, 284 
gum exudate in, 259 
hard and soft teeth in, 262 
heredity in, 266 
history of, 241 

clinical, 294 
hypersensitive dentin in, 304. 

See Hypersensitive dentin, 
inception of, 244, 257, 273, 294 
interglobular spaces in, 287 
lactates formed in, 284 
lactic acid in, 247 
leukemia and, 268 
liquefaction foci in, 285 
loss of crown by, 352 

of root by, 353 

canal continuity in, 
353 

of tissues in, 289 
mentality and, 300 
Miller's general experiments 

on, 245 
morbid anatomy of, 273 
mucin in, 244, 263, 269 
of Nasmyth's membrane, 279 
nervous exhaustion in, 268 
oral hygiene in, 258, 268 
pathology of, 273 
penetrating, 297 
perforation by, 298, 350 
periodicity in, 267, 298 
pigmentation in, 293 
pregnancy and, 263, 268 
prenatal influence in, 266 
prognosis of, 304 
progress of, 274, 295 

saliva in, 263, 264 
prophylaxis of, 268, 272, 358, 

747 
pulp in, almost exposed, 342 

exposed, 303, 346 
recurrence of, 357 
relative liability of teeth to,275 
retention of form in, 295 
roughness of teeth in, 261 
saliva in, 263, 269, 270 
school children and, 268, 300 
secondary, 278, 286, 296, 298 

of dentin, 297 
simple, 339 
spreading, 297 
stages of, 337 



Caries, dental, strengthening of root in, 
354 
structure of teeth in, 261 
sugar in blood and, 270 
sulphocyanate in, 269, 270 
superficial, 337 
symmetry of, 260 
symptoms of, 301 
systemic effects of, 299 
of temporary teeth, 354 
terminations of, 298 
therapeutics of, 271, 337 
transparent zone in, 290 
tube casts in, 289 
tubules in, 281 
typhoid and, 268 
under fillings in, 288 
water and, 262, 267 
xerostoma and, 264 
Caseation, 58, 556, 718 
Castor oil, use of, 78 
Cataphoresis, use of, 327, 391, 433, 496, 

787 
I Cataplasma kaolini, use of, 112, 532 
Cathartics, use of, 78, 85, 527 
| Caush, tubes of, in enamel, 145, 261 
Caustics, use of, 331 
| Cautery, actual, use of, 335 

electric, use of, 351 
Cavitine, use of, 340, 342, 344 
Cells, causes of disease in, 18 
giant, Figs. 17, 24, 45, 202 
life conditions of, 18 
phagocytic, 495 
stimulation of, effects of, 19 
Cellulitis, forms of, 532, 739 
Cement substance, 141 
solution of, 275 
oxychlorid of zinc. See Zinc, 
oxy-eugenol, 345. See also Zinc and 

Eugenol. 
oxyphosphate of copper. See Cop- 
per, 
oxysulphate of zinc. See Zinc, 
silicate, use of. See Silicate, 
zinc phosphate. See Zinc. 
Cemental nodule, 184 
Cementum in dental caries, 259, 293, 
298 
formation of, 93, 143 
histology of, Figs. 128, 134 
malformations of, microscopic, 154 
nutritional relation to dentin, 145, 

Figs. 126, 128 
relation of, to enamel, 145, Fig. 144 
repair of, 229 
i Chalk mixture, use of, 79 
use of, 223, 335, 336 
i Chancre of hands, 730 

of mouth, 729 
I Cheek, distention of, by air pressure, 
504 
swelling of, 109, 519, 526, 531, 533 
Chemotaxis, 41 



INDEX 



807 



Chewing gum, use of, 757 

Chlorazen, use of, 493 

Chloral, use of, 84, 313 

Chlorin, use of, 496, 508 

Chloroform, use of, 85, 109, 312, 325, 

332, 335, 357, 391, 404, 409, 500 
Chloro-percha, use of, 344, 467 
Chlorophyll, 235 
Chlorosis, 23 
Cholesterin, 556, 629 
Chorea from dental disease, 578 

from dentition, 107 
Chromic acid, use of, 615 
Chromogenic bacteria, 237 
Cinchona, use of, 131 
Cinnamon, oil of, use of, 131, 336, 614, 

627, 683 
Circulation, disturbances of, 33 
Clasps, use of, 591 
Cleansing of teeth, 237, 638, 748 
Cleft palate, embryology of, 133 
Clot, absorption of, 28, 38, 56 

healing under, 56 

septic, 27, 28 
Cloudy swelling, 58 
Cloves, oil of, use of, 323, 335, 344, 391, 

420, 614 
Coagulants, use of, 30 
Coagulation of blood, 24, 38 

necrosis, 52 
Cobalt, use of, 440, 441 
Cocain, systemic effects of, 433 

use of, 326, 327, 328, 331, 391, 429, 
431, 433, 438 
Codein, use of, 405 
Coffee, use of, 433 
Cold, as a test, 484 

use of, 527, 532, 570, 616 
Colloid degeneration, 59, 427 
Coloboma, 138 
Colophony, use of, 335, 469 
Combination fillings, use of, 343, 352, 

356 
Compress, use of, 30, 112, 533 
Concrescence of teeth, 171 
Conical teeth, 168, 197 
Constipation, dental pain from, 717 
Contacts, approximal, 341, 355 
Convulsions, cause of, 74 
Copper amalgam, use of, 346, 479 

cones, use of, 468 

ions, use of, 496 

oxyphosphate of, use of, 107, 335, 
338, 345, 346, 352, 355, 356, 479, 
750 

sulphate, use of, 344 
Cord, dental, Fig. 118 
Cotton root dressings, 460, 491, 500 

tampons, danger of, 530, 564 
Counterirritants, use of, 391, 504, 572 
Counterpressure, method of, 525 

in opening tooth, 525 
Cresol, use of. Sve Formocresol. 
Crowns, cantilever, use of, 352, 611 



Crowns, loss of, by caries, 299, 352, Fig. 
300 
in root treatment, 448 
removal of, 501, 509 
temporary, 510 
use of, 352 
Cup, gum, use of, 548 

rubber, use of, 642 
Curette, use of, 562, 616, 774 
Cusps, supplemental, 181 
Cysts, associated with apical conditions, 
539, 556 
causes of, 188, 544 
dentigerous, 117, 188 
dermoid, 189 

teeth in, 189 
impacted teeth as cause of, 117, 128 
varieties of, 117, 128, 544 



Deafness, dental cause of, 578, 715 
Decalcification of dentin in dental caries, 
280 
of roots, 89 
Degeneration, 33 
atrophic, 60 
calcareous, 62, 377, 417 
coUoid, 59, 427 
fatty, 57, 424 

of pulp, 424 
fibroid, 421, 599 
forms of, 57 
granular, 58 
of gum margins, 625 
of nerve-end of pulp, 427 
of pericementum, 589, 599 
of pulp, 420 
Dehydrator, use of, 324 
Dens in dente, 175 
Dentalone, use of, 391 
Dentifrice, use of, 755 
Dentin, destruction of, 89, 199, 214, 280 
cement substance of, 141 
secondary, 361 
development of, 141 
globules, 141 

granular layer of, Fig. 134 
histology of, Figs. 122, 123, 133, 

134, 135 
hypersensitivity of, 209, 304 
after replantation, 367 
anatomical basis of, 304 
causes of, 306 
diagnosis of, 311 
pathology of, 306 
symptoms of, 309 
treatment of, 311 
interglobular spaces in, 151, Figs. 

133, 297 
intertubular substance in, 142 
lines in, 153 
malformations of, microscopic, 150 



INDEX 



Dentin, nutritional relation of, to 
cementum, 147 
recalcification of, 343 
repair of, 229, 366 
resorption of, 89, 400, 581 
secondary, 361 

bacterial penetration of, 368 
staining of, 232, 293 

by putrefaction, 490, 505 
stains of, treatment of, 232, 505 
tubes of, Figs. 122, 123 
tubular calcification of, 359 
tumor of, 365 
Dentinal fibrils, 141 
in enamel, 144 
in interglobular spaces, 151 
papilla, 141 
Dentition, 63 

bottle feeding in, 73, 86 

cause of, 64 

constitutional states modifying, 85 

normal, 63, 87 

pathological, 69, 91 

as cause of epilepsy, 71 

convulsions in, 74, 107 

diagnosis of, 73 

diet in, 79 

headache in, 74 

hemophilia in, 30, 77 

hemorrhage after, 76 

intestinal complications in, 72, 
78 
feeding after, 79 

lancing in, 75 

nervous disturbances in, 73 

paralysis in, 75 

prophylaxis of, 759 

pulmonary disturbances in, 75 

rickets in, 86 

scurvy in, 86 

shock in, after lancing, 77 

skin disorders in, 75, 78 

strabismus in, 75 

symptoms of, 70, 71 

syphilis in, 85 

systemic conditions influenc- 
ing, 70, 85, 106 

treatment of, 75 
periods of, 67 
process of, 66 
second, 87 

cancer from, 1 10 

disorders of, 103 

irregularities of, 92, 94, 101, 
106 

necrosis in, 106 

pathological, 106 
symptoms of, 106 
Depletion of gum, 405 
of pulp, 395, 404 
Derivation, use of, 405, 527, 570, 572 
Dermoid cysts, 189 

teeth in, 189 
Development of face, 133 



Development of teeth, 141 
Devitalization of pulp, 435 
Devitalizing fiber, use of, 404, 430, 441 
Dewey, views of, 555 
Diabetes mellitus, 270 
Diagnosis, definition of, 18 
Diapedesis, 28, 39, 393 
Diathesis, hemorrhagic, 29 
Dichloramin-T, use of, 467, 493, 494, 

497 
Diet, dental caries and, 253 

in pathological dentition, 79 
Dilaceration of teeth, 177 
Diphtheria, 725 

Discoloration of teeth, 488, 490, 505 
Disease, basis of, 17 

causes of, 18 

clinical history of, 18 
Disking teeth, 337, 357 
Dislocation of teeth, 600 
Distomolar, 195 
Disuse of teeth, 595 
Dobell's solution, use of, 552 
Donaldson cleaners, use of,«451 
Dover's powders, use of, 528 
Downie broaches, use of, 452, 500 
Drill, Gates-Glidden, use of, 455 

spear, use of, 450, 525 
Drugs, intoxication by, 618 
Dry cups, use of, 548 

socket, 530, 579 
Dryness, use of, 323, 336 
Dunn syringe, use of, 682 
Dwarfism of teeth, 167 
Dystrophies of teeth, 133, 155 



Ear. disease of, from dental cause, 578, 

715 
Eburnation, 210 

in dental caries, 292 
Ecchymosis, 28 
Eczema, 735 
Electricity in pulp putrefaction, 496 

as test, 485 

uses of, 783 
Electrolysis, 327, 788 
Electrolytic medication, 496, 788 
Embalming paste, use of, 475 
Emboli, septic, 27, 743 
Embolism, 27 
Embryology of face, 133 

of teeth, 141 
Emetin, use of, 684, 688 
Emigration of corpuscles, 37 
Emphysema of cheek from air pressure, 

504 
Empyema of antrum, 542, 550, 717 
Enamel, agenesia of, 166 

curve in temporary teeth, 150 

in dental caries, 273 

dentinal fibrils in, 144 



INDEX 



809 



Enamel development of, 141 

formation of, effect of exanthemata 

upon, 159 
fracture of, 224 
globules, 141 
histology of, 142 
hypoplasia of, 158 
imbrications of, 148 
interprismatic cement, 141 
lines of Schreger in, 148 
malformation of, macroscopic, 142 

microscopic, 143 
mottled, 155 
nodule, 179 
opaque spots in, 155 
organ, 141 

use of, 306 
relation of, to cementum, 306 
resorption of, 214 
rod, 141 

sensitivity of, 310 
stains upon, 234 
strise of, 147 
stripes of Retzius in, 147 

of Schreger in, 148 
tubes, Caush's, 145 
unusual location of, 179 
Endamcebse as cause, 651 
Endarteritis obliterans, 623 
Endocarditis, 743 
Enemata, use of, 85 
Epithelioma from teeth, 110, 209, 736 
Epizootic stomatitis, 724 
Equinia, 725 
Ergot, use of, 31 
Erosion of teeth, 214 
acids in, 216 

extraneous, 220 
diagnosis of, 221 
effects of, 221 

malnutrition upon, 217 
treatment of, 223 
Eruption of teeth, causes of. See Den- 
tition. 
Erythrophlein, use of, 447 
Escat's nasal anesthesia method, 322 
Ether, use of, 312, 325, 357, 376, 428, 

433 
Ethyl chlorid, use of, 325, 376, 420, 529, 

531 
Etiology, definition of, 18 
Eucalyptol, use of, 500, 613, 614, 627 
Euca-percha, use of, 472 
Eugenol, use of, 335, 391, 409, 430, 447, 

478, 539. See Oil of cloves. 
Euroform, use of, 445 
Europhen, use of, 445 
Evans' root drier, use of, 505 
Exanthemata, 726 

malformations caused by, 159 
necrosis caused by, 106 
Excess of teeth, 197 
Exercise, use of, 625 
Exostosis of alveolar process, 578 



Extirpation of pulp, 447 
Extravasation of blood. See Blood. 
Exudates, character of, 35, 37, 38, 40, 44 
Eye, disease of, from dental cause, 715 



Face, development of, 132 

embryology of, 132 

fistula on, treatment of, 553 
Faradism as test, 485, 791 

as therapy, 785 
Fat, degeneration of, 57 

infiltration of, Figs. 25 and 61 

necrosis of, 52 
Feeding in gingivitis, 625 

in malformations, 148 

in pathological dentition, 79 
Ferric chlorid, use of, 262, 532 
Fever, 532 

Fevers, eruptive. See Exanthemata. 
Fiber, arsenical, use of, 404 
Fibrin, formation of, 25 
Fibrosis. See Degeneration. 
Files, root, use of, 452, 468 
Fillings, combination of, 342, 352, 356 
Fistulae, 44 

in antrum, 542 

causes of, 542, 544 

on face, threatened, 533 
treatment of, 553 

healing of, 548 

making artificial, 528 

non-healing of, 548 

packing, 531 

premature closure of, 531, 545, 548 
Flagg's operation for scar, 554 
Flavors, use of, 336 
Fletcher's carbolized resin, use of, 350 
Flexion of teeth, 178, 184 
Floss silk, use of, 750, 753 
Fluctuation, 45 
Food supply, abnormal, 18 
Foramina, delta-like, 454, 475 

open, 472, 504 
Formaldehyde, action of, upon products 
of putrefaction, 499 

irritation from, 500, 609 

uses of, 409, 430, 467, 482, 495, 539, 
546, 614 
Formocresol, use of, 409, 430, 495, 498, 

539, 546, 563 
Formopercha, use of, 472 
Fourth molar, 195 
Fowler's solution, use of, 616 
Fracture of alveolar process, 600 

of teeth, 225, 492 
repair of, 229 
treatment of, 229 
Freezing, use of, 434 
Fungous gum, 419 
Furunculosis, 744 
Fusion of teeth, 169 



S10 



INDEX 



Gall-stones, origin of, 62, 630 
Galvanism as test, 485 
Gangrene, 51, 481 

dry, 51, 482 

moist, 51, 487 

discoloration from, 505 

of pulp, 481 
dry, 482 
moist, 487 
partial, 525 
Gaultheria, oil of, use of, 614, 683 
Gemination of teeth, 175 
Geranium-formol, use of, 498 
Germicides, efficiency of , 493, 793 
Giantism of teeth, 167 
Gingivitis, 603 

antiseptic washes in, 613 

astringent washes in, 613 

deeply seated, 616 

interstitial, 616 

marginal, 604 

systemic causes of, 618 
Glanders, 725 

Glands, pericemental, Fig. 573 
Glycerin, use of, 85, 324, 613, 614 
Glycerophosphates, use of, 223 
Glycogen in caries, 254 
Glycothymoline, use of, 614 
Gonorrhea of mouth, 610, 734 
Gout, 700 

Grafting sponge, use of, 473 
Granulations in regeneration, 52 
Granulomata, 488, 491, 497, 513, 555 

radiography in, 562 

systemic complications, 557 
Greenfield's artificial root, 625 
Gilmore attachment, 594 
Grippe. See Influenza. 
Grooved teeth, 159 
Guards, use of, 527 
Guillotine, gum, 111 
Gum, anatomy of, 604 

function of, 625 

fungous, 419 

hyperplastic, 419 

laceration of, 601 

lancing of, 75, 531 

marginal atrophy of, 625 
Harlan's method in, 626 

sarcoma of, 419 

tissue, action of arsenic on, 528 
Gutta-percha, eucalyptol solution of, 
use of, 472 

solvents of, 500 

use of, 339, 345, 348, 352, 355, 390, 
467, 469 

H 

Hair, teeth and, 189, 193 
Halisteresis ossium, 50, 623 
Hamamelis distillate, use of, 531, 570, 
614 



Hands, sterilization of, 796 
Hare-lip, 138 

Harlan's method in atrophy, 626 
Hartzell, Henri ci, views, 488, 555 
Headache from dental diseases, 128, 746 

in dentition, 74 

from impaction, 128 
Healing of tissue, 52 
Heat in inflammation, 40, 411, 533 

use of, 325, 336, 484, 531, 601, 616 
Hemoglobin, derivatives of, 29, 505 
Hemophilia, 29 

in dentition, 30, 77 
Hemoplastin, use of, 32 
Hemorrhage, acetanilid as cause of, 30 

after extraction, 601 
pulp removal, 431 

treatment of, 30 

varieties of, 24, 28 
Hemorrhagic diathesis, 29, 77 
Herpes labialis, 735 

yOC'i'OT* y O Pv 

Hertwig, root sheath of, 152, 180, 556, 

Figs. 186, 575, 576 
Heteroplasty following amputation of 

natural roots, 671 
High-frequency current, 550, 684, 786 

as a test, 484 
Hot water, use of, 325, 531, 601, 616. 

See Heat. 
How appliance, use of, 466 
Howe on caries bacteria, 250 

silver root filling, 475, 477, 493, 497, 
548 
Howship's lacuna?, 584, Fig. 17 
Hutchinson's teeth, 160 
Hydrogen dioxid, 78, 87, 108, 110, 238, 
239, 409, 420, 456, 534, 546, 
549, 554, 615, 642 
dangers of, 541 
Hydronaphthol, use of, 342, 344, 349, 

613, 629 
Hygiene, definition of, 19 
Hyoscyamin, use of, 314 
Hyperacidosis, 209, 213, 218, 621, 700 
Hypercementosis, 155, 210, 575 

reflex neuroses from, 578, 710 
Hyperemia, arterial, 34, 37 
degrees of, 34 
from arsenic, 435 
of pulp, 380 

arterial, 380 

devitalization in, 392 

from electric action, 387 

from hypercementosis, 578 

idiopathic, 387 

reflex in constructive disease, 

363 
thermal toleration in, 392 
venous, 392 

devitalization in, 438 
from hanging, 395 
suffusion from, 393 
as a resistance to infection, 34 



INDEX 



811 



Hyperemia, results of, 34, 35 

symptoms of, 34, 395 

venous, 34, 37, 392 
Hypernutrition, 19 
Hyperplasia of gum, 419 

of pulp, 415 
Hypersensitivity of dentin, 304. See 

Dentin. 
Hypertrophy of pulp, 415 
Hypnotism, use of, 314 
Hyponutrition, 19 
Hypophosphites, use of, 400 
Hypoplasia, J33 

of enamel, 150, 158 
Hysteria, 314 



Ichthyol, use of, 726 
Immunity to caries, 266 

acquired. See Vaccines. 
Impaction of teeth, 108, 115, 116 
death of pulp from, 128 
diagnosis of, 129 
headache from, 128 
necrosis from, 121 
nervous and cerebral disturb- 
ance from, 128 
neuralgia from, 126 
resorption of roots from, 129 
suppurations from, 109, 123, 

127 
symptoms of, 126 
treatment of, 129 
Implantation, 781 
Inclusion of teeth, 175 
Indican as an index for malnutrition, 620 
Indol, 489, 620 
Infants, feeding of, 79 
Infarction, 27, 28 

of pulp, 393, 420 
Infection, classes of, 41 

from foci, 557, 694, 741, 747 
from the mouth, 741, 748 
general septic, 47, 741 
of mouth, 721 
Infiltration, 61 
calcareous, 62 
fatty, 57 

pigmentary, 28, 61 
Inflammation, 36. See Impaction, Pul- 
pitis, Gingivitis, Pyorrhea, Sto- 
matitis, 
bacteria in, 36, 41, 47 
bloodletting in, 405, 531, 534, 666 
of bone, 48 
catarrhal, Fig. 11 
causes of, 36 
coagulation in, 38 
derivation in, 392, 405 
elements in, 38 
exudates of, 38, 40 
infective, 41 . 
necrosis in, 42 



Inflammation, pathology of, 36 
of pulp, 396 

chronic, 415 
resolution in, 42 
simple, 36 
stimulation in, 528 
suppurative, 42 
symptoms of, 40, 45, 46 
zones in, 39, 45 
Influenza, 385, 717 

dental pain from, 717 
Injury of teeth, mechanical, 224 
Insanity from dental disease, 128, 578, 

715, 746 
Insomnia from dental disease. See 

Focal Infections. 
Instruments, sterilization of, 799. See 

Asepsis. 
Insulator, the, 231 
Interglobular spaces, 151 
Intermaxillary bone, failure of develop- 
ment of, 138 
formation of, 136 
Intestinal complications in pathological 

dentition, 72, 78 
Intoxications. See Acidosis, Drugs, 

Sepsis, Septicemia, Toxemia. 
Intubation of root, 509 
Involucrum, 51 

Iodin, dental, tincture of, 391, 420, 504, 
572 749 
trichforid of, use of, 110, 111, 466, 

756 
use of, 107, 111, 238, 334, 420, 446, 
465, 531, 614, 616, 642, 683, 800 
Iodoform, use of, 344, 349, 467, 469, 475, 

476, 500, 541, 546, 549 
Iodoglycerol, use of, 531, 552, 683, 800 
Ions, definition of, 327, 787 

use of, 684 
Ionization, use of, 496, 563, 787 
Iritis, 746 
Iron, chloride of, tincture of, use of, 

262, 532, 758 
Ischemia, 33 
Ivy, views of, 556 



Jaw, development of, 133 

growth of, cause of, 89 
Jodoformagen, use of, 344, 345, 349, 390, 

391, 447 
Joining of teeth, 589, 592 
Jugulation of pulp, 395 



Kalium natrium, use of, 465, 503, 572 
Kowarska's paste, 571, 673 
Krameria, use of, 613 



812 



INDEX 



Laceration of soft tissues, 601 

Lactic acid, use of, 682 

Lacunae, Howship's, 584, Fig. 17 

Lancing, use of, 75, 110, 531 

Lanolin, use of, 730 

Laudanum, use of, 107, 601 

Lavoris, use of, 614 

Laxatives, use of, 624 

Lead, oral effects of, 622 

Leeches, use of, 527 

Lemon juice, use of, 87, 220, 336, 694 

Leprosy, 739 

Leukemia, 23, 268 

Leukocytosis, 23, 46 

Leukoplakia buccalis, 736 

Lichen planus, 737 

Ligature, use of, 30, 570 

Light, electric, use of, 301, 484, 533, 551 

Lime-water, use of, 758 

Linings, use of, 343 

Listerine, use of, 79, 531, 614 

Lithia salts, use of, 625 

Looseness, effects of, 569 

Ludwig's angina, 110, 739, 742 

Lugol's solution, 552, 615 

Lupus of mouth, 734 

Luxation of teeth, 599 

Lymph, coagulable, 504 

Lymphadenitis, 744 

Lymphangitis, 744 



M 



Magnesia, milk of, use of, 223, 336 

sulphate of, use of, 111, 527 
Magnet, use of, 465 
Malaria, dental pain from, 385, 716 
Malformations, 133 

dystrophic, 155 

macroscopic, 155 

microscopic, 143 

non-dystrophic, 167 

of roots, 182, 460 
Malnutrition, causes of, 18, 741, 745 
Malocclusion of teeth, 98, 569, 588, 593 
classification of, 98 
prophylaxis of, 758 
Malpositions of teeth, 115 
Massage, use of, 109, 532 

vibratory, 533, 785 
Mastication in therapeutics, 626 
Maxillae, embryology of, 133 
Measles, effect of, 106, 159 
Mechanical injury of teeth, 224 

union of teeth, 175. See also Frac- i 
ture. 
Meckel's cartilage, 140 
Melancholia from dental disease, 128, 

746 
Menthol, use of, 323, 325, 334, 391, 409, 
539, 579, 613, 717 



Menthol-phenol, use of, 391, 572 
Mercury, bichlorid of, use of, 456, 469, 
532, 572, 615, 756 

as cause of stomatitis, 572, 721 

oral effects of, 106, 572 

succinamide of, 561, 689 

Talbot's experiments on dogs with, 
568, 573, 619 
Metallic stains, 252 
Metastasis, 27, 44, 47, 48, 743 
Methyl chlorid, use of, 325, 420 
Microorganisms, as disease causes, 18 
Milk of magnesia, use of, 223, 336 

modified, 79 
Molars, pathological dentition of, 106 
Morphin, use of, 313, 405, 527 
Motor reflexes from dental disease, 714 
Mouth, actinomycosis of, 734 

asepsis of, 747, 799 

breathing, 102 

development of, 133 

gangrene of, 109, 725 

gonorrhea of, 610, 734 

infections of, 719 

inflammation of. See Stomatitis. 

lamp, use of. See Light. 

sepsis from, 741 

soft tissues of, laceration of, 601 

sterilization of, 613, 799 

syphilis of, 728 

tuberculosis of, 733 

washes, application of, 613, 755 
Mucin in dental caries, 244, 263, 269 

in saliva, 631 
Mucous anesthesia, 321 

membrane, glycogen in, 265 
Mummification of pulp, 476 
Mummifying paste, arsenic and, 445 

use of, 475, 476 
Myers' syringe, use of, 330 
Myrrh, tincture of, use of, 616 



N 



Nasal anesthesia method, 321 

obstructions, 99, 102 
Nasmyth's membrane, Figs. 186, 577 

in dental caries, 279 
Necrobiosis, 50, 57 
Necrosis, 50 

after extraction, 602 
of alveolar bone, 530 
of bone, 50 

arsenical, 444 

from alveolodental abscess, 

553 563 
from syphilis, 563, 732 
coagulation, 52 
etiology of, 50 
of fat, 52 

from exanthemata, 106 
from mercury, 106, 572 
from typhoid fever, 106 
liquefaction, 52 



INDEX 



813 



Necrosis, phosphorus and, 737 

varieties of, 42, 44 
Needle, hypodermic, 315 
breakage of, 321 
Neoplasm of pulp, 426 
Neosalvarsan, use of, 690 
Nephritis, 744 
Nerve, fifth, 707 

sensory, of face, 707 

supply, abnormal, 18 

vasomotor, 33, 380 
Nervocidin, use of, 326, 434 
Nervous disturbances in dental disease, 
746 
in dentition, 74, 107 
Neuman, sheath of, Figs. 122, 123 
Neuralgia, cause of, 109, 299, 705 

from hypercementosis, 578 

from hypersensitive dentin, 706 

from impacted teeth, 712 

from pericemental disease, 710 

from pulp disease, 708 

from root resorption, 589 

treatment of, 717 
Neuritis, 744 
Neuroses, reflex, 705 
Nitric acid, use of, 335 
Nitrous oxid gas, use of, 312, 404, 428, 

531 
Nodule, cemental, 184 

enamel, 179 

in pulp, 369 
Noma, 109, 725 
Non-conductors, uses of, 340 
Nose and dental disease, 543 
Novocain, use of, 110, 315, 390, 391, 429 

431, 438, 531, 572, 601 
Number of teeth, variations in, 192 
Nutrition, basis of, 19 

deficiency of, 33 



Ocean water, use of, 552 
Odontalgia, phantom, 712 
Odontoblasts, 67, 141 

atrophy of, 364 

relation of, to sensory nerves, 304 
Odontomata, 184 
Odor as a test, 484 
Oligocythemia, 21 
Olive oil, use of, 78 
Opium, use of, 78, 79, 109 
Opsonic index, raising of, 690 
Orange juice, use of, 87 
Orthoform, use of, 334, 351, 445, 603 
Oscillation, 38 
Osteitis, condensing, 49 

rarefying, 48 
Osteodentin, 367 
Osteomalacia, 623 
Osteomyelitis, 48 
Osteoporosis, 48 



Osteosclerosis, 49, 120 
Overarch bar, use of, 592 
Overuse of teeth, 588 
Oxalic acid, use of, 239 
Oxygen, nascent, use of, 507 



Pain, dental, from other sources than 
dental, 716 

postextraction, 579, 601 
Palate, cleft, cause of, 137 
Paraffin, use of, 466, 494, 509 

solvent of, 500 
Paraform, use of, 476 
Paraglossus, the, 213 
Paralysis in dentition, 75 

from dental disease, 578 
Paramolar, 195 
Pathology, basis of, 19 

dental, definition of, 17 

general, definition of, 17 
Peck's anesthetic method, 322 
Pediluvium, hot, use of, 527 
Perforation by accident, 464 

by caries, 298, 350 

as cause of abscess of root, 550 

filling of, 464, 479 
Pericemental abscess, 698 
Pericementitis, 511. See also Pyorrhea 
alveolaris. 

acute, septic, apical, 512 
extraction in, 529 

beginning at gum margin, 605 

chronic, septic, apical, 535, 567 

non-septic, 376, 568 
results of, 574 
symptomatic, 572 

septic at bifurcations of roots, 567 

symptomatology of, 511 

traumatic, 568 
Pericementum, degeneration of, 589 
fibroid, 599 

development of, 143 

diseases of, 511 

fibrosis of, 599 

glands of, 556 

histology of, Figs. 575, 576, 577 

overuse of, 588 
Periostitis, 48 

maxillary, 545 
Petechia, 28 
Phagocytosis, 604 
Phantom odontalgia, 712 
Phenacetin, use of, 405 
Phenandyne, use of, 391 
Phenobromate, use of, 313 
Phenol camphor, use of, 323, 391, 539, 
572, 601, 683 

sodique, use of, 78, 107, 601, 614, 
756 

use of, 332, 334, 391, 434, 723. See 
Carbolic acid. 



814 



INDEX 



Phenolsiilphonic acid, use of, 497, 546, 

563 
Phosphor necrosis, 737 
Phosphorus, use of, 223 
Physical condition, abnormal, 18 
Picks, Rhein's, use of, 452, 466 
Pigmentary infiltration, 393, 438, 506 
Pigmentation in dental caries, 293 
Pigments in tissue, 28 
Pilocarpin, oral effects of, 573 
Pins, removal of, 501 
Piscidia erythrina, use of, 313 
Pitted teeth, 159 
Plantation, 777 

mode of attachment in, 587 

resorption after, 587 
Plaques, microbic. See Caries. 
Plaster of Paris, use of, 349 
Plethora, 21 
Pocket for arsenic, 405 
Podophyllin, use of, 624 
Pointing, 43, 45, 531 
Porcelain inlays, use of, 345, 627 
Porte-polisher, use of, 645, 750, 754 
Potassium bitartrate, use of, 756 

bromid, use of, 213 

carbonate, use of, 324 

chlorate, use of, 78,' 87, 616, 756 

hydrate, use of, 332 

iodid, use of, 391, 573, 621 

sulphocyanate, use of, 336 
Potassocain, use of, 325 
Poultices, danger of, 533 
Powder, tooth, use of, 755 
Pregnancy, dental pain from, 717 
Pressure anesthesia, 326, 330, 404, 410 

hemorrhage after, 431 
Procain, use of. See Novocain.- 
Process, alveolar, fracture of, 600 
v Prognosis, definition of, 18 
Prophylaxis, 19, 596, 749, 751 
Protozoa as disease causes, 653 
Pulp, abscess of, 410 

access of bacteria to, 386, 397 

action of arsenic on, 521 

almost exposed, 342 

anesthesia of, 429 

atrophy of, 364, 423 

capping of, 348 

cavity, duplication of, 175 

forms of, Figs. 418, 419, 420 

constructive diseases of, 359 

death of, from impaction, 128 

degeneration of, 368 

calcific, 377, 414, 417 
cloudy, 424 
colloid, Fig. 388 
fatty, 424 
fibroid, 420 
nerve, Fig. 389 

depletion of, 395 

destructive diseases of, 380 

devitalization of, 425, 447 

digestion of, 479 



Pulp, exposure of, 346 
extirpation of, 447 
fungous, 416 
gangrene of, 481 
partial, 409 
hyperemia of, 380 
arterial, 380 

devitalization in, 392 
from electric action, 387 
idiopathic, 385 
pericementitis from, 388 
thermal toleration in, 392 
uterus . and bladder as 
cause of, 711 
from arsenic, 435 
test for, 389 
venous, 389 

suffusion in, 438 
hyperplasia of, 415 
infarction of, 422 
inflammation of, 396. See Pulpitis. 

chronic, 415 
jugulation of, 395 
knocking out, 446 
moist gangrene of, 487 
mummification of, 476, 482 
neoplasm of, 427 
nodules, 369, 386 
arsenic and, 375 
reflexes from, 375 
polypus of, 416 
protection of, 343 
puncturing of, 395, 404, 410, 414 
putrefaction of, 409, 487 
removal of, 428 
partial, 477 

special methods of, 446 
replantation of, vitality after, 367 
sclerosis of, 415 
sedation of. See Sedatives, 
suffusion, 393, 438 
suppuration of, 406 
thermal tolerance of, 392 
thrombosis of, 422 
toughening of, 455 
ulceration of, 407 
vessels, paralysis of, 396 
vitality of, tests for, 483 
Pulpitis, 396 
acute, 398 
chronic, 415 

from pyorrhea, 397, 663 
hyperplastic, 415 
reflex disorder from, 708 
resorption of dentin in, 400 
Pumice, use of, 643 
Puncture probe, 446 
Puncturing of pulp, 395, 404, 410, 414, 

446 
Purpura hemorrhagica, 741 
Pus formation, 42 

varieties of, 44 
Putrefaction of pulp, 487 
Pyemia, 47 



INDEX 



815 



Pyogenic calculus, 544, 556, 628 

Pyorrhea alveolaris, 649 

abscess secondary to, 664, 698 
beginning with a marginal gin- 
givitis, 657 
Bier's hyperemia in, 685 
in bifurcations of roots, 670 
breath in, 669 

bridge and plates in, 678, 682 
causes of, 649, 659 
clinical history of, 656, 659 
dental caries and, 665 
diagnosis of, 662 
endarteritis in, 663 
gum incision in, 669 
heteroplasty of roots in, 671 
interstitial gingivitis in, 660 
living pulps and, 661, 665, 670 
looseness in, 661 
not dependent upon calculus, 

696 
oral catarrh in, 662 
pathology of, 637 
predisposition to, 569, 572, 

599, 607, 625 
prevention of motion in, 672 
prophylaxis in, 666, 686 
radiography in, 662, 761 
recurrence of, 687 
replantation in, 685 
root amputation in, 670 
splints for use in, 673 
surgery in, 669 
systemic effects of, 694 
treatment of, 666 

medicinal, 682, 688 

Pyrozone, use of, 238, 438, 465, 503, 507 



Quinin, use of, 313, 405, 527, 532, 719 



Rachitis, 86 

effects of, 150 
Radiography, 761 

as a test, 487, 531, 538, 562, 578, 
587, 662 

of root canal. See Root and Canal. 
Raisin, roasted, use of, 528 
Rapid breathing, use of, 314 
Recalcification of dentin, 343 
Reflex action, 385 

disorders of dental origin, 705 
of systemic origin, 718 

neuroses, 705 
Regeneration of tissue, 52 
Removable crowns, 509 
Repair of dentin and cementum, 229 
Replantation, 550, 777 

of pulp, vitality after, 367 



Replantation, secondary dentin after, 
367 
of teeth, 777 
Resistance to infection, impaired, 745 
Resolution, 42 

Resorption of bone, 48, 50, 583, 623 
of enamel, 214 
perforation by, 92, 400 
of permanent roots, 581 
of temporary roots, 89 
Rest, surgical, 527, 570 

use of, 32, 570, 593, 625 
Retention of teeth, 92. See Impaction. 
Retzius, stripes of, in enamel, 147 
Rheumatism, 745 
Rhigolene, use of, 325 
Ringer solution, use of, 315 
Robinson's remedy, use of, 332, 336, 339 
Rollin's knife, 529 

Root, amputation of, 670, 671, 771, 776 
artificial, 781 
buried, 299 

calcification of, Figs. 35, 50 
canal, accidents in opening, 464 
anatomy of, 452, 456 
asepsis of, 448 
electrical disinfection of, 496, 

788 
filling of, 466, 479, 534 
inaccessible foramina of, 452 
loss of continuity of, 462 
radiography of, 448, 453, 467, 

469, 561, 764 
with open foramina, 472 
development of, 67, 93 
drier, Evans', use of, 446 
end capping, 469, 471 
extraction of, in hypercementosis, 

578 
filling, disappearance of, 474 

removal of, 500 
fracture from putrefaction, 492 
fusion and concrescence, 169, 171 
implantation of, 781 
intubation, 509 
long and short, 168 
loss of, by caries, 353, 462 
malformations of, 182 
multiple, 183 

perforation, 298, 350, 464, 479, 550 
permanent, formation of, 93 

resorption of, 581 
repair of, 324 
replantation of, 647 
resorption of, 89 

of permanent, 581 
sterilization of, 448, 493, 503 
systematic stopping, 540 
temporary, resorption of, 89 
transplantation of, 779 
Rose geranium, oil of, use of, 498 
Rubber band, use of, 753 
cup, use of, 548, 641 
sore mouth and, 724 



816 



INDEX 



Saccharin, use of, 78, 131, 613 
Salicylic acid, use of, 613 
Saliva, analysis of, 631 

in dental caries, 263, 269, 270 

glucose in, 268 

increased flow of, 757 

lack of, 264 

relation of acid food to, 756 
Salivary calculus, 630. See Calculus. 
Salivation by mercury, 572 
Salol, use of, 79, 532 
Salt, 309, 402, 601, 683 
Salvarsan, use of, 615, 654, 690 
Sandarac, use of, 350, 420 
Sanguinary calculus, 628, 647 
Scab, healing under, 56 
Scar, threatened, 533 

tissue, 535 
Scarlet fever, effect of, 106, 159 
Schreger, stripes of, in dentin, 154 

in enamel, 148, 153 
Scissors, gum, use of, 76, 111 
Sclerosis of pulp, 415 
Scorbutus, 738, 739 

infantile, 86 

oral effects of, 572, 738 
Scurvy. See Scorbutus. 
Second intention, healing by, 52 
Secondary dentin. See Dentin. 
Sedation, results of, 19 
Sedatives, use of, 391, 404, 570, 572 
Seidlitz powders, 624 
Senility and gums, 625 
Sensitivity as test, 483 
Sepsis, general, of dental origin. See 
Infection. 

intoxication from. See Infection. 
Septicemia, 44, 47, 48, 51, 106, 109 

from apical abscess, 519 
Sequestrum, 51 
Serres, glands of, Fig. 515 
Serum therapy, 31 
Serumal calculus, 628, 647 
Shellac, use of, 131 
Shock, 77 
Silicate cements, use of, 166, 224, 238, 

339, 346 
Silver cones, use of, 468 

nitrate, use of, 210, 331, 333, 338, 
355, 390, 420, 553, 615, 723, 
750 

root filling (Howe), 475, 477 
Sinus, 44 

Size of teeth, variations in, 167 
Skin eruptions, 75 
Slough, 52 

Soap, use of, 546, 624 
Sodium biborate, use of, 613, 614 

bicarbonate, use of, 223, 332, 336, 
342, 344, 404, 625 

bromid, use of, 84, 213 

carbonate, use of, 797 



Sodium chlorid, use of, 223, 333, 465, 
616, 625 

dioxid, danger of, 503, 572 

use of, 238, 239, 332, 503, 507 

hydrate, use of, 332, 376 

ions, use of, 496 

phosphate, use of, 223 

potassium and, alloy of, use of, 465, 
503, 572 
Somnoform, use of, 313, 428, 531 
Sphacelus, 52 

Spirochetes, 608, 654, 690, 740 
Splints, use of> 570, 595, 673 
Stains, black, 236 

in dentin, 237 

dyes and, 236 

green, 234 

metallic, 232 

non-metallic, 234 

red, 237 

tobacco, 236 

treatment of, 237 
Staphylococci, 406, 411, 655, 690 
Stasis of blood, 38 
Steresol, use of, 131 
Sterilization, dental, 793 
Stimulation, effects of, 19 
Stomatitis, 719 

aphthous, 722 

classification of varieties of, 719 

in dentition, 70, 78 

diphtheritic, 725 

epizootic, 724 

equinis, 725 

from drugs, 728 

from eruptive fevers, 726 

from glanders, 725 

from rubber plates, 724 

gangrenous, 725 

gonorrheal, 610, 734 

herpetic, 735 

infective catarrhal, 720 

mercurial, 573, 622, 721 

beneficial effects of mercurv in, 
573 

simple catarrhal, 720 

symptomatic catarrhal, 721 

syphilitic, 728 

tubercular, 733 

typhoid, 106 

ulcerative, 610, 721, 725 
Stopping, systematic, 540 
Strabismus in dentition, 75 
Streptococci, 406, 411, 654 
Strontium lactate, use of, 31 
Structure of teeth, 143, 261 
Strychnin, use of, 433, 718 
Subgingival calculus, 628, 644 
Suffusion, 28, 393 

from arsenic, 438 

from hanging, 395 

from venous hyperemia, 393 
Sugar in diabetes, 270 
Suggestion, use of, 312, 314 



INDEX 



817 



Sulphocyanate, use of, 270 

Sulphur, use of, 683 

Sulphuric acid, use of, 239, 376, 430, 
446, 464, 465, 507, 549, 572, 682 

Sulphurous acid, use of, 508 

Supernumerary teeth, 197 

Supplemental cusps, 181 

Suppuration in inflammation, 42 
of pulp, 406 

Suprarenin, use of, 315 

Symptoms, definition of, 18 

Synostosis, dental, 579 

Syphilis, dental pain from, 385, 716 
hereditary, 162 
of mouth, 728 

necrosis of bone from, 563, 732 
oral effects of, 164, 573, 728 
stigmata of, 160, 164, 181 

Syphilitic teeth, 148, 160 

Syringes, use of, 315, 432, 546, 554, 682 

Systematic stooping of troublesome 
root, 540 

Systemic disease from focal infection. 
See Infection, 
prophylaxis of, 758 



Talcum, use of, 78 

Talon on tooth, 182 

Tannin, use of, 30, 324 

Tapping, as test, 487, 539 

Tartasol, use of, 682 

Temperature, natural tolerance of, 392 

Temporary stopping, use of, 467 

Tents, use of, 531, 533 

Tests for asepsis, 503 

for pulp vitality, 483 

Tetanic spasm from teeth, 209 

Therapeutics, basis of, 17, 20 

Thoma, view of, 555 

Thrombosis, 25, 422 

Throphleol, use of, 447 

Thymol, use of, 341, 344, 348, 349, 390, 
391, 396, 405, 409, 420, 614 

Thymophen, use of, 391 

Tic douloureux, 375 

Tomes, granular layer of, Fig. 134 J 

Toxemia, 47, 73. See also Septicemia. 

Translucency as a test, 484 

Transparency of dental structures, 199, 
290, 766 

Transparent zone, 290 

Transplantation, 779 

Trephine, use of, 529 

Treponema pallidum, 728 

Trichloracetic acid, use of, 420, 618, 682 
723 

Trigemin, use of, 405, 528 

Trioxymethylene, use of, 334 

Trophic disturbance from dental dis- 
ease, 7X6 



Tube casts in dental caries, 289 
Tuberculosis of mouth, 733 
Tubes of dentin, Figs. 122 to 136 

of enamel, 144 
Tubular calcification, 359 
Tumors, 191 

dental pain from, 385 
Turkish baths, use of, 629 
Typhoid fever, effect of, 106, 268 



Ulceration, 42, 46 

of pulp, 407, 410 
Union of teeth, mechanical, 175 
Urates in pericementum, 699 
Uterine disease, dental pain from, 717 
Uvula, bifid, 138 



Vaccine therapy, 112, 532, 541, 554, 

690 
Vacuum appliances, 546 
Vapocain, use of, 325 
Varnish, use of, 340 
Vascular system, disturbances of, 21 
Vasomotor nerves, 33 
Venous hyperemia, 34, 37, 392 
Veratrin, use of, 109 
Vermifuges, use of, 214 
Vernas lotion, use of, 6X4 
Vibration, electric, 785 

use of, 533, 785 
Vincent's angina, 608, 615, 740 
Violet ray, 484, 550, 785 



W 



Wall, follicle, 143 

Wassermann test, 182 
Waste, removal, abnormal, 18 
Water, boiling, as germicide, 794, 797 

drinking of, 625 

warm, use of, 339 
Wax, use of, 474 

Whisky, use of, 314. See Brandy. 
Wintergreen, oil of, use of, 336 
Wood point, use of, 750, 754 



X-rays, use of, 684, 718. See Radiog- 
raphy. 
Xerostomia, 264 
Xylol, use of, 500 



818 



INDEX 



Zinc chlorid, use of, 324, 331, 332, 336, 
340, 420, 431, 504, 572, 613, 614, 
615, 683 

cones, use of, 472 

iodide, use of, 614, 683 

ions, use of, 496, 787 

ointment, use of, 78 



Zinc oxid and eugenol, use of, 345, 349, 
355, 390, 391, 479 
use of, 344, 349 
oxychlorid of, use of, 344, 345, 349, 

472 
oxyphosphate, use of, 107, 340, 342, 

344, 346, 348, 355, 390, 499 
oxysulphate, use of, 326, 345, 349 
sulphate, use of, 391 
sulphocarbolate, use of, 683 



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